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Year 2 Medicine > Innate Immune Defences & Inflammation 2: The Induced Response > Flashcards

Innate Immune Defences & Inflammation 2: The Induced Response Flashcards

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1
Q

Cells of the innate & adaptive immune system

  • The discovery of innate lymphoid cells (ILCs) is blurring the traditional boundaries between innate and adaptive immune systems. Invariant natural killer T cells, some B cells at epithelial barriers (B1 cells) and gamma delta T cells have innate qualities whereas NK cells may adapt after their first encounter with a pathogen due to innate immune memory. T and B cells also have innate immune receptors such as TLRs.
A
  • The discovery of innate lymphoid cells (ILCs) is blurring the traditional boundaries between innate and adaptive immune systems. Invariant natural killer T cells, some B cells at epithelial barriers (B1 cells) and gamma delta T cells have innate qualities whereas NK cells may adapt after their first encounter with a pathogen due to innate immune memory. T and B cells also have innate immune receptors such as TLRs.
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2
Q

Innate immune cells

  • What cells are involved? What do they do?
A
  • Neutrophils - Phagocytosis, Antimicrobial peptides, Reactive oxygen and nitrogen species
  • Macrophages - Phagocytosis, Antimicrobial peptides, Reactive oxygen and nitrogen species, Inflammatory mediators, antigen presentation, cytokines, complement proteins
  • Dendritic cells - Antigen presentation, Costimulatory signals, Reactive oxygen species, Interferon, Cytokines
  • Natural Killer cells - Lysis of viral-infected cells, Interferon, Macrophage activation, Granzyme, Perforin
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3
Q

What are the functions of a neutrophil?

A
  • Phagocytosis, Antimicrobial peptides, Reactive oxygen and nitrogen species
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4
Q

What are the functions of a macrophage?

A
  • Phagocytosis, Antimicrobial peptides, Reactive oxygen and nitrogen species, Inflammatory mediators, antigen presentation, cytokines, complement proteins
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5
Q

What are the functions of dendritic cells?

A
  • Antigen presentation, Costimulatory signals, Reactive oxygen species, Interferon, Cytokines (Plasmacytoid dendritic cells (DCs) are of lymphoid origin, Myeloid DCs are of myeloid origin - plasmacytoid DCs produce large amounts of type 1 IFN whereas for myeloid DCs the main role is antigen presentation)
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6
Q

What are the functions of natural killer cells?

A
  • Lysis of viral-infected cells, Interferon, Macrophage activation, Granzyme, Perforin (Perforin is pore forming permitting entry of granzyme into cells where it induces apoptosis)
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7
Q

… is pore forming permitting entry of granzyme into cells where it induces apoptosis.

A

Perforin is pore forming permitting entry of granzyme into cells where it induces apoptosis.

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8
Q

Plasmacytoid dendritic cells (DCs) are of … origin

A

Plasmacytoid dendritic cells (DCs) are of lymphoid origin

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9
Q

Myeloid DCs are of … origin

A

Myeloid DCs are of myeloid origin

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10
Q

… DCs produce large amounts of type 1 IFN whereas for … DCs the main role is antigen presentation

A

plasmacytoid DCs produce large amounts of type 1 IFN whereas for myeloid DCs the main role is antigen presentation

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11
Q

Phagocyte recruitment

  • … produced by macrophages dilate local blood vessels and increase endothelial adhesion molecule expression.
  • … attract monocytes and neutrophils to the infection
  • Cell adhesion molecules (ICAM-1 and VCAM-1) are upregulated on the endothelium which bind to integrins (family of adhesion molecules) on the leukocytes
A
  • Cytokines produced by macrophages dilate local blood vessels and increase endothelial adhesion molecule expression.
  • Chemokines attract monocytes and neutrophils to the infection
  • Cell adhesion molecules (ICAM-1 and VCAM-1) are upregulated on the endothelium which bind to integrins (family of adhesion molecules) on the leukocytes
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12
Q

Phagocyte recruitment

  • Cytokines produced by macrophages … local blood vessels and … endothelial adhesion molecule expression.
  • Chemokines attract monocytes and … to the infection
  • Cell adhesion molecules (ICAM-1 and VCAM-1) are upregulated on the endothelium which bind to integrins (family of adhesion molecules) on the leukocytes
A
  • Cytokines produced by macrophages dilate local blood vessels and increase endothelial adhesion molecule expression.
  • Chemokines attract monocytes and neutrophils to the infection
  • Cell adhesion molecules (ICAM-1 and VCAM-1) are upregulated on the endothelium which bind to integrins (family of adhesion molecules) on the leukocytes
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13
Q

Phagocyte recruitment

  • Cytokines produced by macrophages dilate local blood vessels and increase endothelial adhesion molecule expression.
  • Chemokines attract monocytes and neutrophils to the infection
  • Cell … molecules (ICAM-1 and VCAM-1) are upregulated on the endothelium which bind to integrins (family of … molecules) on the leukocytes
A
  • Cytokines produced by macrophages dilate local blood vessels and increase endothelial adhesion molecule expression.
  • Chemokines attract monocytes and neutrophils to the infection
  • Cell adhesion molecules (ICAM-1 and VCAM-1) are upregulated on the endothelium which bind to integrins (family of adhesion molecules) on the leukocytes
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14
Q

Phagocyte recruitment

  • Cytokines produced by macrophages dilate local blood vessels and increase endothelial adhesion molecule expression.
  • Chemokines attract monocytes and neutrophils to the infection
  • Cell adhesion molecules (…-1 and …-1) are upregulated on the endothelium which bind to integrins (family of adhesion molecules) on the leukocytes
A
  • Cytokines produced by macrophages dilate local blood vessels and increase endothelial adhesion molecule expression.
  • Chemokines attract monocytes and neutrophils to the infection
  • Cell adhesion molecules (ICAM-1 and VCAM-1) are upregulated on the endothelium which bind to integrins (family of adhesion molecules) on the leukocytes
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15
Q

Phagocytosis is performed by …, … cells and …

A

Phagocytosis is performed by neutrophils, dendritic cells and macrophages

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16
Q

Neutrophils, Dendritic Cells and Macrophages all perform…

A

phagocytosis

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17
Q

Phagocytosis is the … and … of … particles

A

Phagocytosis is the capture and digestion of foreign particles

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18
Q

Phagocytosis is the … and … of … particles

A

Phagocytosis is the capture and digestion of foreign particles

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19
Q

What is phagocytosis?

A

Phagocytosis is the capture and digestion of foreign particles

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20
Q

… are proteins of the innate and adaptive immune system that facilitate phagocytosis and cell lysis by “marking” antigen.

A

Opsonins are proteins of the innate and adaptive immune system that facilitate phagocytosis and cell lysis by “marking” antigen.

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21
Q

Complement components (C3b) and Collectins (Mannose-binding lectin) and antibodies are all good examples of …

A

opsonins (opsonins are proteins of the innate and adaptive immune system that facilitate phagocytosis and cell lysis by “marking” antigen.)

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22
Q

Opsonins engage with … receptors (complement receptors, fc receptors, Mannose receptor, Scavenger receptors)

A

Opsonins engage with phagocytic receptors (complement receptors, fc receptors, Mannose receptor, Scavenger receptors)

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23
Q

… receptors recognize bacteria, viruses and apoptotic cells

A

Scavenger receptors recognize bacteria, viruses and apoptotic cells

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24
Q

The complement receptor CR1 binds to … (complement component)

A

The complement receptor CR1 binds to C3b (complement component)

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25
C-type-lectin receptors (Dectin-1 & mannose receptor) help ... bacteria. Mannose Receptor binds mannose and fructose residues of glycans (polysaccharides).
C-type-lectin receptors (Dectin-1 & mannose receptor) help **phagocytose** bacteria. Mannose Receptor binds mannose and fructose residues of glycans (polysaccharides).
26
_Receptor mediated phagocytosis_ * ... receptors bind to opsonins * Microorganisms are internalised by receptor-mediated endocytosis * Fusion of ... with lysosome forms a phagolysosome in which microorganisms are degraded
* **Phagocytic** receptors bind to opsonins * Microorganisms are internalised by receptor-mediated endocytosis * Fusion of **endosome** with lysosome forms a phagolysosome in which microorganisms are degraded
27
_Receptor mediated phagocytosis_ * Phagocytic receptors bind to opsonins * Microorganisms are internalised by receptor-mediated endocytosis * Fusion of endosome with ... forms a ... in which microorganisms are degraded
* Phagocytic receptors bind to opsonins * Microorganisms are internalised by receptor-mediated endocytosis * Fusion of endosome with **lysosome** forms a **phagolysosome** in which microorganisms are degraded
28
_Receptor mediated phagocytosis_ * Phagocytic receptors bind to ... * Microorganisms are internalised by receptor-mediated endocytosis * Fusion of endosome with lysosome forms a phagolysosome in which microorganisms are degraded
* Phagocytic receptors bind to **opsonins** * Microorganisms are internalised by receptor-mediated endocytosis * Fusion of endosome with lysosome forms a phagolysosome in which microorganisms are degraded
29
_Receptor mediated phagocytosis_ * Phagocytic receptors bind to opsonins * Microorganisms are internalised by receptor-mediated ... * Fusion of endosome with lysosome forms a phagolysosome in which microorganisms are degraded
* Phagocytic receptors bind to opsonins * Microorganisms are internalised by receptor-mediated **endocytosis** * Fusion of endosome with lysosome forms a phagolysosome in which microorganisms are degraded
30
Lysosomes can fuse with ... to form a ...
Lysosomes can fuse with **phagosomes** to form a **phagolysosome**
31
_Antimicrobial mechanisms of phagocytes_ * Within phagolysosome: * ... environment - ... pH * Oxygen and nitrogen derived products - break down pathogens * Antimicrobial ... are present * Enzymes such as lysozyme - digests cell walls of some gram+ bacteria * Lactoferrin - binds Fe2+ which is needed for bacterial growth (competitor)
* Within phagolysosome: * **Acidic** environment - **Low** pH * Oxygen and nitrogen derived products - break down pathogens * Antimicrobial **peptides** are present * Enzymes such as lysozyme - digests cell walls of some gram+ bacteria * Lactoferrin - binds Fe2+ which is needed for bacterial growth (competitor)
32
_Antimicrobial mechanisms of phagocytes_ * Within phagolysosome: * Acidic environment - Low pH * Oxygen and nitrogen derived products - break down pathogens * Antimicrobial peptides are present * Enzymes such as ... - digests cell walls of some gram+ bacteria * Lactoferrin - binds Fe2+ which is needed for bacterial growth (competitor)
* Within phagolysosome: * Acidic environment - Low pH * Oxygen and nitrogen derived products - break down pathogens * Antimicrobial peptides are present * Enzymes such as **lysozyme** - digests cell walls of some gram+ bacteria * Lactoferrin - binds Fe2+ which is needed for bacterial growth (competitor)
33
_Antimicrobial mechanisms of phagocytes_ * Within phagolysosome: * Acidic environment - Low pH * Oxygen and nitrogen derived products - break down pathogens * Antimicrobial peptides are present * Enzymes such as lysozyme - digests cell walls of some gram... bacteria * ... - binds Fe2+ which is needed for bacterial growth (competitor)
* Within phagolysosome: * Acidic environment - Low pH * Oxygen and nitrogen derived products - break down pathogens * Antimicrobial peptides are present * Enzymes such as lysozyme - digests cell walls of some **gram+** bacteria * **Lactoferrin** - binds Fe2+ which is needed for bacterial growth (competitor)
34
_Antimicrobial mechanisms of phagocytes_ * Within phagolysosome: * Acidic environment - Low pH * ... and ... derived products - break down pathogens * Antimicrobial peptides are present * Enzymes such as lysozyme - digests cell walls of some gram+ bacteria * Lactoferrin - binds Fe2+ which is needed for ... ...
* Within phagolysosome: * Acidic environment - Low pH * **Oxygen** and **nitrogen** derived products - break down pathogens * Antimicrobial peptides are present * Enzymes such as lysozyme - digests cell walls of some gram+ bacteria * Lactoferrin - binds Fe2+ which is needed for **bacterial growth (competitor)**
35
_Neutrophil Extracellular Traps (NETs)_ * When activated some neutrophils undergo a special form of cell death termed ‘...’ * During ... nuclear chromatin is released from cells trapping microorganisms thus aiding phagocytosis
* When activated some neutrophils undergo a special form of cell death termed ‘**NETosis**’ * During **NETosis** nuclear chromatin is released from cells trapping microorganisms thus aiding phagocytosis
36
_Neutrophil Extracellular Traps (NETs)_ * When activated some neutrophils undergo a special form of cell ... termed ‘NETosis’ * During NETosis nuclear chromatin is released from cells trapping microorganisms thus aiding phagocytosis
* When activated some neutrophils undergo a special form of cell **death** termed ‘NETosis’ * During NETosis nuclear chromatin is released from cells trapping microorganisms thus aiding phagocytosis
37
_Neutrophil Extracellular Traps (NETs)_ * When activated some neutrophils undergo a special form of cell death termed ‘NETosis’ * During NETosis nuclear ... is released from cells trapping microorganisms thus aiding phagocytosis
* When activated some neutrophils undergo a special form of cell death termed ‘NETosis’ * During NETosis nuclear **chromatin** is released from cells trapping microorganisms thus aiding phagocytosis
38
_Neutrophil Extracellular Traps (NETs)_ * When activated some neutrophils undergo a special form of cell death termed ‘NETosis’ * During NETosis nuclear chromatin is released from cells trapping microorganisms thus aiding ...
* When activated some neutrophils undergo a special form of cell death termed ‘NETosis’ * During NETosis nuclear chromatin is released from cells trapping microorganisms thus aiding **phagocytosis**
39
During NETosis nuclear ... is released from cells trapping microorganisms thus aiding phagocytosis
During NETosis nuclear **chromatin** is released from cells trapping microorganisms thus aiding phagocytosis
40
During NETosis nuclear chromatin is released from cells trapping microorganisms thus aiding ...
During NETosis nuclear chromatin is released from cells trapping microorganisms thus aiding **phagocytosis**
41
When activated some neutrophils undergo a special form of cell death termed ‘...’
When activated some neutrophils undergo a special form of cell death termed ‘**NETosis**’
42
_Pattern recognition receptors (PRRs)_ * How many families of PRRs are there? * What are they called?
* 5 families * **C type lectin receptors (CLRs), Toll-like receptors (TLRs), NOD-like receptors (NLRs), Rig-I like receptors (RLRs), Cytosolic DNA sensors (CDS)**
43
_Pattern recognition receptors (PRRs)_ * How many families of PRRs are there? * What are they called?
* 5 families * **C type lectin receptors (CLRs), Toll-like receptors (TLRs), NOD-like receptors (NLRs), Rig-I like receptors (RLRs), Cytosolic DNA sensors (CDS)**
44
**Below are all different families of what?** * C type lectin receptors (CLRs) * Toll-like receptors (TLRs) * NOD-like receptors (NLRs) * Rig-I like receptors (RLRs) * Cytosolic DNA sensors (CDS)
Pattern recognition receptors (PRRs)
45
... ... ... (...s) are receptors able to recognise conserved structures
**Pattern recognition receptors (PRRs)** are receptors able to recognise conserved structures
46
Pattern recognition receptors (PRRs) recognise patterns termed: ...-associated ... ... (...s)
Pattern recognition receptors (PRRs) recognise patterns termed: **pathogen-associated molecular patterns (PAMPs)**
47
What do Pattern recognition receptors (PRRs) recognise ?
**patterns termed: pathogen-associated molecular patterns (PAMPs)**
48
_Pattern-associated molecular patterns (PAMPs) & DAMPs_ * PAMPs - Microbes evolve rapidly, so innate immunity must focus on highly ... and ... components of microbes (cell wall structures; nucleic acids) * DAMPs – Damage associated molecular patterns; molecules released from necrotic cells
* PAMPs - Microbes evolve rapidly, so innate immunity must focus on highly **conserved** and **essential** components of microbes (cell wall structures; nucleic acids) * DAMPs – Damage associated molecular patterns; molecules released from necrotic cells
49
_Pattern-associated molecular patterns (PAMPs) & DAMPs_ * PAMPs - Microbes evolve rapidly, so innate immunity must focus on highly conserved and essential components of microbes (cell wall structures; nucleic acids) * DAMPs – ... associated molecular patterns; molecules released from ... cells
* PAMPs - Microbes evolve rapidly, so innate immunity must focus on highly conserved and essential components of microbes (cell wall structures; nucleic acids) * DAMPs – **Damage** associated molecular patterns; molecules released from **necrotic** cells
50
DAMPs – ... associated ... patterns; molecules released from necrotic cells
DAMPs – **Damage** associated **molecular** patterns; molecules released from necrotic cells
51
_C type lectin receptors (CLRs)_ * CLRs are expressed by most cell type that phagocytose glycoproteins and microbes for antigen presentation to T lymphocytes * CLRs bind to ... in a calcium-dependent manner * Type I CLRs assist with antigen uptake by phagocytes * Type II CLRs are involved in fungal recognition * Soluble CLRs include MBL that binds ... on pathogen surfaces
* CLRs are expressed by most cell type that phagocytose glycoproteins and microbes for antigen presentation to T lymphocytes * CLRs bind to **carbohydrates** in a calcium-dependent manner * Type I CLRs assist with antigen uptake by phagocytes * Type II CLRs are involved in fungal recognition * Soluble CLRs include MBL that binds **carbohydrates** on pathogen surfaces
52
_C type lectin receptors (CLRs)_ * CLRs are expressed by most cell type that phagocytose glycoproteins and microbes for antigen presentation to T lymphocytes * CLRs bind to carbohydrates in a ...-dependent manner * Type I CLRs assist with antigen uptake by phagocytes * Type II CLRs are involved in ... recognition * Soluble CLRs include MBL that binds carbohydrates on pathogen surfaces
* CLRs are expressed by most cell type that phagocytose glycoproteins and microbes for antigen presentation to T lymphocytes * CLRs bind to carbohydrates in a **calcium**-dependent manner * Type I CLRs assist with antigen uptake by phagocytes * Type II CLRs are involved in **fungal** recognition * Soluble CLRs include MBL that binds carbohydrates on pathogen surfaces
53
_C type lectin receptors (CLRs)_ * CLRs are expressed by most cell type that phagocytose glycoproteins and microbes for antigen presentation to T lymphocytes * CLRs bind to carbohydrates in a calcium-dependent manner * Type I CLRs assist with ... uptake by phagocytes * Type II CLRs are involved in fungal recognition * Soluble CLRs include MBL that binds carbohydrates on pathogen surfaces
* CLRs are expressed by most cell type that phagocytose glycoproteins and microbes for antigen presentation to T lymphocytes * CLRs bind to carbohydrates in a calcium-dependent manner * Type I CLRs assist with **antigen** uptake by phagocytes * Type II CLRs are involved in fungal recognition * Soluble CLRs include MBL that binds carbohydrates on pathogen surfaces
54
CLRs are expressed by most cell type that ... glycoproteins and microbes for ... presentation to T lymphocytes
CLRs are expressed by most cell type that **phagocytose** glycoproteins and microbes for **antigen** presentation to T lymphocytes
55
CLRs bind to ... in a calcium-dependent manner
CLRs bind to **carbohydrates** in a calcium-dependent manner
56
Type I CLRs assist with antigen uptake by ...
Type I CLRs assist with antigen uptake by **phagocytes**
57
Type II CLRs are involved in ... recognition
Type II CLRs are involved in **fungal** recognition
58
Soluble CLRs include ... that binds carbohydrates on pathogen surfaces
Soluble CLRs include **MBL** that binds carbohydrates on pathogen surfaces
59
_Drosophila Toll Receptors_ * Mutagenesis work on Drosophila revealed two members of the Toll family, dToll and 18-wheeler (dont need to know) * Important for ... * Important for immunity to the fungal and bacterial infections * Mammalian equivalent are the Toll-like receptors (TLRs)
* Mutagenesis work on Drosophila revealed two members of the Toll family, dToll and 18-wheeler (dont need to know) * Important for **development** * Important for immunity to the fungal and bacterial infections * Mammalian equivalent are the Toll-like receptors (TLRs)
60
_Drosophila Toll Receptors_ * Mutagenesis work on Drosophila revealed two members of the Toll family, dToll and 18-wheeler (dont need to know) * Important for development * Important for immunity to the fungal and bacterial infections * Mammalian equivalent are the ...-... receptors
* Mutagenesis work on Drosophila revealed two members of the Toll family, dToll and 18-wheeler (dont need to know) * Important for development * Important for immunity to the fungal and bacterial infections * Mammalian equivalent are the **Toll-like receptors (TLRs)**
61
_Drosophila Toll Receptors_ * Mutagenesis work on Drosophila revealed two members of the Toll family, dToll and 18-wheeler (dont need to know) * Important for development * Important for immunity to the ... and ... infections * Mammalian equivalent are the Toll-like receptors (TLRs)
* Mutagenesis work on Drosophila revealed two members of the Toll family, dToll and 18-wheeler (dont need to know) * Important for development * Important for immunity to the **fungal** and **bacterial** infections * Mammalian equivalent are the Toll-like receptors (TLRs)
62
_Toll-like receptor structure_ * Extracellular: * ... domain – site of pathogen binding * Cytosolic side: * TIR-domain - conserved stretch of ~200 amino acids
* Extracellular: * **LRR** domain – site of pathogen binding * Cytosolic side: * TIR-domain - conserved stretch of ~200 amino acids
63
_Toll-like receptor structure_ * Extracellular: * LRR domain – site of ... binding * Cytosolic side: * TIR-domain - conserved stretch of ~200 amino acids
* Extracellular: * LRR domain – site of **pathogen** binding * Cytosolic side: * TIR-domain - conserved stretch of ~200 amino acids
64
_Toll-like receptor structure_ * Extracellular: * LRR domain – site of pathogen binding * Cytosolic side: * ...-domain - conserved stretch of ~200 amino acids
* Extracellular: * LRR domain – site of pathogen binding * Cytosolic side: * **TIR**-domain - conserved stretch of ~200 amino acids
65
_Toll-like receptor structure_ * Extracellular: * LRR domain – site of pathogen binding * ... side: * TIR-domain - conserved stretch of ~200 amino acids
* Extracellular: * LRR domain – site of pathogen binding * **Cytosolic** side: * TIR-domain - conserved stretch of ~200 amino acids
66
TLRs form functional .../...dimers
TLRs form functional **hetero/homodimers**
67
_Cellular location of TLRS_ * TLR-2 and TLR-6 recognise ... lipopeptides (heterodimer) * TLR-2 and TLR-1 recognise ... lipopeptides (heterodimer) * TLR-5 recognise flagellin * TLR-4 recognise LPS on coat of gram- bacteria - works with MD-2 * The rest within endosome - recognise nucleic acid structures (TLRs 3, 7, 8, and 9 are situated in the membranes of endosomes and lysosomes) * TLR10 is predominantly endosomal recognising dsRNA
* TLR-2 and TLR-6 recognise **diacyl** lipopeptides (heterodimer) * TLR-2 and TLR-1 recognise **triacyl** lipopeptides (heterodimer) * TLR-5 recognise flagellin * TLR-4 recognise LPS on coat of gram- bacteria - works with MD-2 * The rest within endosome - recognise nucleic acid structures (TLRs 3, 7, 8, and 9 are situated in the membranes of endosomes and lysosomes) * TLR10 is predominantly endosomal recognising dsRNA
68
_Cellular location of TLRS_ * TLR-2 and TLR-6 recognise diacyl lipopeptides (heterodimer) * TLR-2 and TLR-1 recognise triacyl lipopeptides (heterodimer) * TLR-5 recognise ... * TLR-4 recognise LPS on coat of gram- bacteria - works with MD-2 * The rest within endosome - recognise nucleic acid structures (TLRs 3, 7, 8, and 9 are situated in the membranes of endosomes and lysosomes) * TLR10 is predominantly endosomal recognising dsRNA
* TLR-2 and TLR-6 recognise diacyl lipopeptides (heterodimer) * TLR-2 and TLR-1 recognise triacyl lipopeptides (heterodimer) * TLR-5 recognise **flagellin** * TLR-4 recognise LPS on coat of gram- bacteria - works with MD-2 * The rest within endosome - recognise nucleic acid structures (TLRs 3, 7, 8, and 9 are situated in the membranes of endosomes and lysosomes) * TLR10 is predominantly endosomal recognising dsRNA
69
_Cellular location of TLRS_ * TLR-2 and TLR-6 recognise diacyl lipopeptides (heterodimer) * TLR-2 and TLR-1 recognise triacyl lipopeptides (heterodimer) * TLR-5 recongise flagellin * TLR-4 recognise ... on coat of gram- bacteria - works with MD-2 * The rest within endosome - recognise nucleic acid structures (TLRs 3, 7, 8, and 9 are situated in the membranes of endosomes and lysosomes) * TLR10 is predominantly endosomal recognising dsRNA
* TLR-2 and TLR-6 recognise diacyl lipopeptides (heterodimer) * TLR-2 and TLR-1 recognise triacyl lipopeptides (heterodimer) * TLR-5 recongise flagellin * TLR-4 recognise **LPS** on coat of gram- bacteria - works with MD-2 * The rest within endosome - recognise nucleic acid structures (TLRs 3, 7, 8, and 9 are situated in the membranes of endosomes and lysosomes) * TLR10 is predominantly endosomal recognising dsRNA
70
_Cellular location of TLRS_ * TLR-2 and TLR-6 recognise diacyl lipopeptides (heterodimer) * TLR-2 and TLR-1 recognise triacyl lipopeptides (heterodimer) * TLR-5 recongise flagellin * TLR-4 recognise LPS on coat of gram- bacteria - works with MD-2 * The rest within ... - recognise nucleic acid structures (TLRs 3, 7, 8, and 9 are situated in the membranes of ... and lysosomes) * TLR10 is predominantly endosomal recognising dsRNA
* TLR-2 and TLR-6 recognise diacyl lipopeptides (heterodimer) * TLR-2 and TLR-1 recognise triacyl lipopeptides (heterodimer) * TLR-5 recongise flagellin * TLR-4 recognise LPS on coat of gram- bacteria - works with MD-2 * The rest within **endosome** - recognise nucleic acid structures (TLRs 3, 7, 8, and 9 are situated in the membranes of **endosomes** and lysosomes) * TLR10 is predominantly endosomal recognising dsRNA
71
The TLRs include TLR1, TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, TLR10, TLR11, TLR12, and TLR13, though the last ... are not found in humans.
The TLRs include TLR1, TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, TLR10, TLR11, TLR12, and TLR13, though the last **three** are not found in humans.
72
TLR-... and TLR-... recognise diacyl lipopeptides (heterodimer)
**TLR-2 and TLR-6 recognise diacyl lipopeptides (heterodimer)**
73
TLR-... and TLR-... recognise triacyl lipopeptides (heterodimer)
TLR-**2** and TLR-**1** recognise triacyl lipopeptides (heterodimer)
74
TLR-... recognise flagellin
TLR-**5** recognise flagellin
75
TLR-... recognise LPS on coat of gram- bacteria - works with MD-2
TLR-**4** recognise LPS on coat of gram- bacteria - works with MD-2
76
TLRs 3, 7, 8, and 9 are situated in the membranes of ... and ...
TLRs 3, 7, 8, and 9 are situated in the membranes of **endosomes** and **lysosomes**
77
TLR... is predominantly endosomal recognising dsRNA
TLR**10** is predominantly endosomal recognising dsRNA
78
TLR-3 recognises ...-stranded RNA
TLR-3 recognises **double**-stranded RNA
79
TLR-... recognises double-stranded RNA
TLR-**3** recognises double-stranded RNA
80
TLR-... recognises single-stranded RNA
TLR-**7** recognises single-stranded RNA
81
TLR-7 recognises ...-stranded RNA
TLR-... recognises **single**-stranded RNA
82
TLR-8 recognises ...-stranded RNA
TLR-8 recognises **single**-stranded RNA
83
TLR-... recongises CpG DNA
TLR-**9** recongises CpG DNA
84
Cell Surface TLRs (1,2,4,5,6) mainly recognise ... products, but on our own host molecules recognise mainly ... or ... molecules
Cell Surface TLRs (1,2,4,5,6) mainly recognise **bacterial** products, but on our own host molecules recognise mainly **lipid** or **protein** molecules
85
Cell Surface TLRs (which 5?) mainly recognise bacterial products, but on our own host molecules recognise mainly lipid or protein molecules
Cell Surface TLRs **(1,2,4,5,6)** mainly recognise bacterial products, but on our own host molecules recognise mainly lipid or protein molecules
86
... TSRs (3,7,8,9,10) mainly recognise viral products, but on our host molecules recognise our own DNA or RNA (dsRNA, ssRNA, DNA)
**Endosomal** TSRs (3,7,8,9,10) mainly recognise viral products, but on our host molecules recognise our own DNA or RNA (dsRNA, ssRNA, DNA)
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Endosomal TSRs (which 5?) mainly recognise viral products, but on our host molecules recognise our own DNA or RNA (dsRNA, ssRNA, DNA)
Endosomal TSRs (**3,7,8,9,10**) mainly recognise viral products, but on our host molecules recognise our own DNA or RNA (dsRNA, ssRNA, DNA)
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Endosomal TSRs (3,7,8,9,10) mainly recognise viral products, but on our host molecules recognise our own ... and ...
**Endosomal** TSRs (3,7,8,9,10) mainly recognise viral products, but on our host molecules recognise our own **DNA or RNA (dsRNA, ssRNA, DNA)**
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Endosomal TSRs (3,7,8,9,10) mainly recognise ... products, but on our host molecules recognise our own DNA or RNA (dsRNA, ssRNA, DNA)
Endosomal TSRs (3,7,8,9,10) mainly recognise **viral** products, but on our host molecules recognise our own DNA or RNA (dsRNA, ssRNA, DNA)
90
TLRs recognise ... and ... ligands
TLRs recognise **exogenous** and **endogenous** ligands
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_TLR signalling cascade_ * TLR signalling induces genes that function in host defense: * Pro-inflammatory & anti-inflammatory ... * MHC & co-stimulatory molecules * antimicrobial peptides & complement components
* TLR signalling induces genes that function in host defense: * Pro-inflammatory & anti-inflammatory **cytokines** * MHC & co-stimulatory molecules * antimicrobial peptides & complement components
92
_TLR signalling cascade_ * TLR signalling induces genes that function in host defense: * Pro-inflammatory & anti-inflammatory cytokines * ... & co-stimulatory molecules * antimicrobial peptides & complement components
* TLR signalling induces genes that function in host defense: * Pro-inflammatory & anti-inflammatory cytokines * **MHC** & co-stimulatory molecules * antimicrobial peptides & complement components
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_TLR signalling cascade_ * TLR signalling induces genes that function in host defense: * Pro-inflammatory & anti-inflammatory cytokines * MHC & co-stimulatory molecules * antimicrobial peptides & complement components
* TLR signalling induces genes that function in host defense: * Pro-inflammatory & anti-inflammatory cytokines * MHC & co-stimulatory molecules * antimicrobial peptides & complement components
94
_TLR signalling cascade_ * TLR signalling induces genes that function in host defense: * Pro-inflammatory & anti-inflammatory cytokines * MHC & co-stimulatory molecules * ... peptides & ... components
* TLR signalling induces genes that function in host defense: * Pro-inflammatory & anti-inflammatory cytokines * MHC & co-stimulatory molecules * **antimicrobial** peptides & **complement** components
95
_TLR adaptor proteins_ * Not all Toll-like receptors use all of the adaptor molecules * TLR-... uses all of them * TLR 3 only uses TRIF * All apart from TLR3 use Myd88
* Not all Toll-like receptors use all of the adaptor molecules * **TLR-4 uses all of them** * TLR 3 only uses TRIF * All apart from TLR3 use Myd88
96
At the top of the TLR signalling cascade 4 different adaptive proteins are used. These are ...
At the top of the TLR signalling cascade 4 different adaptive proteins are used. These are **MyD88, MAL, TRIF and TRAM**
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At the top of the TLR signalling cascade 4 different adaptive proteins are used. These are ...
At the top of the TLR signalling cascade 4 different adaptive proteins are used. These are **MyD88, MAL, TRIF and TRAM**
98
_TLR adaptor proteins_ * Not all Toll-like receptors use all of the adaptor molecules * TLR-4 uses all of them * TLR 3 only uses ... * All apart from TLR3 use Myd88
* Not all Toll-like receptors use all of the adaptor molecules * TLR-4 uses all of them * TLR 3 only uses **TRIF** * All apart from TLR3 use Myd88
99
_TLR adaptor proteins_ * Not all Toll-like receptors use all of the adaptor molecules * TLR-4 uses all of them * TLR 3 only uses TRIF * All apart from TLR3 use ...
* Not all Toll-like receptors use all of the adaptor molecules * TLR-4 uses all of them * TLR 3 only uses TRIF * All apart from TLR3 use **Myd88**
100
_TLR adaptor proteins_ * Not all Toll-like receptors use all of the ... molecules * TLR-4 uses all of them * TLR 3 only uses TRIF * All apart from TLR3 use Myd88
* Not all Toll-like receptors use all of the **adaptor** molecules * TLR-4 uses all of them * TLR 3 only uses TRIF * All apart from TLR3 use Myd88
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_MyD88 gain of function mutation_ * Waldenström macroglobulinemia (rare type of non-Hodgkin lymphoma) * MyD88 mutation is present in 90% of patients causing cell growth and survival * B cells make large amounts of ... that can cause excess bleeding, vision problems and headaches * Lymphoma cells proliferating in the bone marrow cause anaemia, neutropenia and thrombocytopenia
* Waldenström macroglobulinemia (rare type of non-Hodgkin lymphoma) * MyD88 mutation is present in 90% of patients causing cell growth and survival * B cells make large amounts of **IgM** that can cause excess bleeding, vision problems and headaches * Lymphoma cells proliferating in the bone marrow cause anaemia, neutropenia and thrombocytopenia
102
_MyD88 gain of function mutation_ * Waldenström ... (rare type of non-Hodgkin lymphoma) * MyD88 mutation is present in 90% of patients causing cell growth and survival * B cells make large amounts of IgM that can cause excess bleeding, vision problems and headaches * Lymphoma cells proliferating in the bone marrow cause anaemia, neutropenia and thrombocytopenia
* Waldenström **macroglobulinemia** (rare type of non-Hodgkin lymphoma) * MyD88 mutation is present in 90% of patients causing cell growth and survival * B cells make large amounts of IgM that can cause excess bleeding, vision problems and headaches * Lymphoma cells proliferating in the bone marrow cause anaemia, neutropenia and thrombocytopenia
103
_MyD88 gain of function mutation_ * Waldenström macroglobulinemia (rare type of non-Hodgkin lymphoma) * MyD88 mutation is present in ...% of patients causing cell growth and survival * B cells make large amounts of IgM that can cause excess bleeding, vision problems and headaches * Lymphoma cells ... in the bone marrow cause anaemia, neutropenia and thrombocytopenia
* Waldenström macroglobulinemia (rare type of non-Hodgkin lymphoma) * MyD88 mutation is present in **90**% of patients causing cell growth and survival * B cells make large amounts of IgM that can cause excess bleeding, vision problems and headaches * Lymphoma cells **proliferating** in the bone marrow cause anaemia, neutropenia and thrombocytopenia
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_MyD88 gain of function mutation_ * Waldenström macroglobulinemia (rare type of non-... lymphoma) * MyD88 mutation is present in 90% of patients causing cell growth and survival * B cells make large amounts of IgM that can cause excess bleeding, vision problems and headaches * ... cells proliferating in the bone marrow cause anaemia, neutropenia and thrombocytopenia
* Waldenström macroglobulinemia (rare type of non-**Hodgkin** lymphoma) * MyD88 mutation is present in 90% of patients causing cell growth and survival * B cells make large amounts of IgM that can cause excess bleeding, vision problems and headaches * **Lymphoma** cells proliferating in the bone marrow cause anaemia, neutropenia and thrombocytopenia
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MyD88 mutation is present in ...% of patients with Waldenström macroglobulinemia (rare type of non-Hodgkin lymphoma) causing cell growth and survival
MyD88 mutation is present in **90**% of patients with Waldenström macroglobulinemia (rare type of non-Hodgkin lymphoma) causing cell growth and survival
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In Waldenström macroglobulinemia, B cells make large amounts of IgM that can cause 3 symptoms - what are they?
**excess bleeding, vision problems and headaches (**MyD88 mutation is present in 90% of patients causing cell growth and survival)
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In Waldenström macroglobulinemia, Lymphoma cells proliferating in the bone marrow cause ..., ... and thrombocytopenia
In Waldenström macroglobulinemia, Lymphoma cells proliferating in the bone marrow cause **anaemia, neutropenia** and thrombocytopenia
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_A life without MyD88?_ * Nine MyD88 deficient children suffered from life-threatening, often recurrent ... bacterial infections, but were otherwise healthy, with normal resistance to other microbes. * Their clinical status improved with ..., possibly due to a compensatory effect of adaptive immunity or other innate immune mechanisms.
* Nine MyD88 deficient children suffered from life-threatening, often recurrent **pyogenic** bacterial infections, but were otherwise healthy, with normal resistance to other microbes. * Their clinical status improved with **age**, possibly due to a compensatory effect of adaptive immunity or other innate immune mechanisms.
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_Are TLRs important?_ * Of the 10 TLRs only deficiency in ... has been linked to immunodeficiency. * TLR-... Deficiency in Patients with Herpes Simplex Encephalitis (HSE) - Inflammation of the brain due to infection with herpes simplex virus (HSV-1) * HSV-1 is a dsDNA virus, but during viral replication it produces dsRNA * Defects in other signalling molecules involved in the TLR3 signalling pathway have also been associated with HSE
* Of the 10 TLRs only deficiency in **TLR3** has been linked to immunodeficiency. * **TLR-3** Deficiency in Patients with Herpes Simplex Encephalitis (HSE) - Inflammation of the brain due to infection with herpes simplex virus (HSV-1) * HSV-1 is a dsDNA virus, but during viral replication it produces dsRNA * Defects in other signalling molecules involved in the TLR3 signalling pathway have also been associated with HSE
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_Are TLRs important?_ * Of the 10 TLRs only deficiency in TLR3 has been linked to immunodeficiency. * TLR-3 Deficiency in Patients with Herpes Simplex Encephalitis (HSE) - Inflammation of the brain due to infection with herpes simplex virus (HSV-1) * HSV-1 is a ...DNA virus, but during viral replication it produces ...RNA * Defects in other signalling molecules involved in the TLR3 signalling pathway have also been associated with HSE
* Of the 10 TLRs only deficiency in TLR3 has been linked to immunodeficiency. * TLR-3 Deficiency in Patients with Herpes Simplex Encephalitis (HSE) - Inflammation of the brain due to infection with herpes simplex virus (HSV-1) * HSV-1 is a **dsDNA** virus, but during viral replication it produces **dsRNA** * Defects in other signalling molecules involved in the TLR3 signalling pathway have also been associated with HSE
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Of the 10 TLRs only deficiency in ... has been linked to immunodeficiency.
Of the 10 TLRs only deficiency in **TLR3** has been linked to immunodeficiency.
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_TLRs in disease_
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_TLRs in disease_
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_TLRs in Infection_ * **...** – TLR8 * **...** – TLR2 and 4 * **T..** – TLR2 and 4
* **HIV** – TLR8 * **Sepsis** – TLR2 and 4 * **Tuberculosis** – TLR2 and 4
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_TLRs in Inflammation (Diseases)_ * Systemic ... ... – TLR7, 8 and 9 * ... Disease – TLR2 and 4 * A... – TLR2 and 4
* Systemic **Lupus Erythematosus** – TLR7, 8 and 9 * **Alzheimer's** Disease – TLR2 and 4 * **Atherosclerosis** – TLR2 and 4
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_TLR agonists - Diseases_ * Infection- genital warts (TLR... ligand - Aldara) * Cancer - Melanoma (TLR... ligand - Aldara) * Allergy – Ragweed pollen (TLR9) * Vaccine adjuvant
* Infection- genital warts (**TLR7** ligand - Aldara) * Cancer - Melanoma (**TLR7** ligand - Aldara) * Allergy – Ragweed pollen (TLR9) * Vaccine adjuvant
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_TLR agonists - Diseases_ * Infection- genital warts (TLR7 ligand - Aldara) * Cancer - Melanoma (TLR7 ligand - Aldara) * Allergy – Ragweed pollen (TLR...) * Vaccine adjuvant
* Infection- genital warts (TLR7 ligand - Aldara) * Cancer - Melanoma (TLR7 ligand - Aldara) * Allergy – Ragweed pollen (**TLR9**) * Vaccine adjuvant
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_TLR agonists - Diseases_ * Infection- genital warts (TLR7 ligand - Aldara) * Cancer - Melanoma (TLR7 ligand - Aldara) * Allergy – Ragweed pollen (TLR9) * ... adjuvant
* Infection- genital warts (TLR7 ligand - Aldara) * Cancer - Melanoma (TLR7 ligand - Aldara) * Allergy – Ragweed pollen (TLR9) * **Vaccine** adjuvant
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_TLR antagonists - Disease_ * ... diseases (TLR7, 8 & 9) * S... (TLR4)
* **Autoimmunity** (TLR7, 8 & 9) * **Sepsis** (TLR4)
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_Nod-like receptors (NLRs)_ * NLR = Nucleotide-binding ... Rich * Cytoplasmic pattern recognition molecules * Two major groups- NLRCs and NLRPs – ‘C’ stands for ‘caspase recruitment domain (CARD)’ and the ‘P’ stands for pyrin domain.
* NLR = Nucleotide-binding **Leucine** Rich * Cytoplasmic pattern recognition molecules * Two major groups- NLRCs and NLRPs – ‘C’ stands for ‘caspase recruitment domain (CARD)’ and the ‘P’ stands for pyrin domain.
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_Nod-like receptors (NLRs)_ * NLR = Nucleotide-binding Leucine Rich * ... pattern recognition molecules * Two major groups- NLRCs and NLRPs – ‘C’ stands for ‘caspase recruitment domain (CARD)’ and the ‘P’ stands for pyrin domain.
* NLR = Nucleotide-binding Leucine Rich * **Cytoplasmic** pattern recognition molecules * Two major groups- NLRCs and NLRPs – ‘C’ stands for ‘caspase recruitment domain (CARD)’ and the ‘P’ stands for pyrin domain.
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_Nod-like receptors (NLRs)_ * NLR = Nucleotide-binding Leucine Rich * Cytoplasmic pattern recognition molecules * Two major groups- NLRCs and NLRPs – ‘C’ stands for ‘caspase recruitment domain (CARD)’ and the ‘P’ stands for ... domain.
* NLR = Nucleotide-binding Leucine Rich * Cytoplasmic pattern recognition molecules * Two major groups- NLRCs and NLRPs – ‘C’ stands for ‘caspase recruitment domain (CARD)’ and the ‘P’ stands for **pyrin** domain.
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What PRRs are only found in the cytoplasm?
Nod-like receptors (NLRs) and RIG-I-like receptors (RLRs)
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What are the two major groups of NLRs?
NLRCs and NLRPs
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_NLRCs_ * Two examples: NLRC1 (...) and NLRC2 (...) * They have a leucine rich domain which can bind to peptidoglycan which is present on the cell membrane of most bacteria
* Two examples: NLRC1 (**NOD1**) and NLRC2 (**NOD2**) * They have a leucine rich domain which can bind to peptidoglycan which is present on the cell membrane of most bacteria
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_NLRCs_ * Two examples: NLRC1 (NOD1) and NLRC2 (NOD2) * They have a ... rich domain which can bind to ... which is present on the cell membrane of most bacteria
* Two examples: NLRC1 (NOD1) and NLRC2 (NOD2) * They have a **leucine** rich domain which can bind to **peptidoglycan** which is present on the cell membrane of most bacteria
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_NOD1 and NOD2_ * NOD1 and NOD2 detect similar yet distinct peptides of ... * NOD1 binds γ-glutamyl diaminopimelic acid (iE-DAP) (Mainly Gm-ve Bacteria) * NOD2 binds muramyl dipeptide (both Gram+ve and Gram-ve bacteria)
* NOD1 and NOD2 detect similar yet distinct peptides of **peptidoglycan** * NOD1 binds γ-glutamyl diaminopimelic acid (iE-DAP) (Mainly Gm-ve Bacteria) * NOD2 binds muramyl dipeptide (both Gram+ve and Gram-ve bacteria)
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_NOD1 and NOD2_ * NOD1 and NOD2 detect similar yet distinct peptides of peptidoglycan * NOD1 binds γ-glutamyl diaminopimelic acid (...-DAP) (Mainly Gm... Bacteria) * NOD2 binds muramyl dipeptide (both Gram+ve and Gram-ve bacteria)
* NOD1 and NOD2 detect similar yet distinct peptides of peptidoglycan * NOD1 binds γ-glutamyl diaminopimelic acid (**iE-DAP**) (Mainly Gm**-ve** Bacteria) * NOD2 binds muramyl dipeptide (both Gram+ve and Gram-ve bacteria)
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_NOD1 and NOD2_ * NOD1 and NOD2 detect similar yet distinct peptides of peptidoglycan * NOD1 binds γ-glutamyl diaminopimelic acid (iE-DAP) (Mainly Gm-ve Bacteria) * NOD2 binds ... dipeptide (both Gram+ve and Gram-ve bacteria)
* NOD1 and NOD2 detect similar yet distinct peptides of peptidoglycan * NOD1 binds γ-glutamyl diaminopimelic acid (iE-DAP) (Mainly Gm-ve Bacteria) * NOD2 binds **muramyl** dipeptide (both Gram+ve and Gram-ve bacteria)
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NOD2 gain of function mutation linked to early onset ... where granulomas develop in the organs of the body.
NOD2 gain of function mutation linked to early onset **sarcoidosis** where granulomas develop in the organs of the body.
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NOD... gain of function mutation linked to early onset sarcoidosis where granulomas develop in the organs of the body.
**NOD2** gain of function mutation linked to early onset sarcoidosis where granulomas develop in the organs of the body.
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NOD2 gain of function mutation linked to early onset sarcoidosis where ... develop in the organs of the body.
NOD2 gain of function mutation linked to early onset sarcoidosis where **granulomas** develop in the organs of the body.
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NOD... loss of function mutation is associated with susceptibility to Crohn’s disease, a chronic intestinal inflammatory disorder
NOD**2** loss of function mutation is associated with susceptibility to Crohn’s disease, a chronic intestinal inflammatory disorder
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NOD2 loss of function mutation is associated with susceptibility to ... disease, a chronic intestinal inflammatory disorder
NOD2 loss of function mutation is associated with susceptibility to **Crohn’s** disease, a chronic intestinal inflammatory disorder
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NOD2 ... of function mutation is associated with susceptibility to Crohn’s disease, a chronic intestinal inflammatory disorder
NOD2 **loss** of function mutation is associated with susceptibility to Crohn’s disease, a chronic intestinal inflammatory disorder
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_NLRPs_ * The best characterised is **NLRP...** (**NALP...**) * NLRP3 is activated by cellular stress; K+ efflux, ATP, reactive oxygen species and lysosomal damage * Inflammasome activation is essential for IL-1 and IL-18 secretion
* The best characterised is **NLRP3** (**NALP3**) * NLRP3 is activated by cellular stress; K+ efflux, ATP, reactive oxygen species and lysosomal damage * Inflammasome activation is essential for IL-1 and IL-18 secretion
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_NLRPs_ * The best characterised is **NLRP...** (**NALP...**) * NLRP3 is activated by ... stress; K+ efflux, ATP, reactive oxygen species and lysosomal damage * Inflammasome activation is essential for IL-1 and IL-18 secretion
* The best characterised is **NLRP3** (**NALP3**) * NLRP3 is activated by **cellular** stress; K+ efflux, ATP, reactive oxygen species and lysosomal damage * Inflammasome activation is essential for IL-1 and IL-18 secretion
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_NLRPs_ * The best characterised is **NLRP...** (**NALP...**) * NLRP3 is activated by ... stress; K+ efflux, ATP, reactive oxygen species and lysosomal damage * ... activation is essential for IL-1 and IL-18 secretion
* The best characterised is **NLRP3** (**NALP3**) * NLRP3 is activated by **cellular** stress; K+ efflux, ATP, reactive oxygen species and lysosomal damage * **Inflammasome** activation is essential for IL-1 and IL-18 secretion
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Activation of the inflammasomes results in the processing and subsequent secretion of the pro-inflammatory cytokines IL-... and IL-...
Activation of the inflammasomes results in the processing and subsequent secretion of the pro-inflammatory cytokines **IL-1 and IL-18.**
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NLRP3 is activated by cellular stress; ...+ efflux, A..., ... oxygen species and lysosomal damage
NLRP3 is activated by cellular stress; **K+ efflux, ATP, reactive oxygen species and lysosomal damage**
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_The Inflammasome senses danger_ * Activated by cellular infection or cell ... * Stress caused by crystals getting stuck or bursting the phagosome during endocytosis (recognised - Uric acid crystals (gout))
* Activated by cellular infection or cell **stress** * Stress caused by crystals getting stuck or bursting the phagosome during endocytosis (recognised - Uric acid crystals (gout))
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_The Inflammasome senses danger_ * Activated by cellular infection or cell stress * Stress caused by ... getting stuck or bursting the phagosome during endocytosis (recognised - Uric acid crystals (...))
* Activated by cellular infection or cell **stress** * Stress caused by **crystals** getting stuck or bursting the phagosome during endocytosis (recognised - Uric acid crystals (**gout**))
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_NALP3 Inflammasome_ * Sensor of damage and cellular ... * ... can form and are taken up by cells - this then drives activation and formation of the NALP3 inflammasome * Conditions/Diseases/Infections such as: Gout, Asbestos, Silica, Amyloid beta (Alzheimer's), Islet amyloid polypetide (T2 diabetes), Hemozoin (Malaria)
* Sensor of damage and cellular **stress** * **Crystals** can form and are taken up by cells - this then drives activation and formation of the NALP3 inflammasome * Conditions/Diseases/Infections such as: Gout, Asbestos, Silica, Amyloid beta (Alzheimer's), Islet amyloid polypetide (T2 diabetes), Hemozoin (Malaria)
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_NALP3 Inflammasome_ * Sensor of damage and cellular stress * Crystals can form and are taken up by cells - this then drives activation and formation of the NALP3 inflammasome * Conditions/Diseases/Infections such as: G..., As..., Silica, Amyloid beta (Alzheimer's), Islet amyloid polypetide (T2 diabetes), Hemozoin (Malaria)
* Sensor of damage and cellular stress * Crystals can form and are taken up by cells - this then drives activation and formation of the NALP3 inflammasome * Conditions/Diseases/Infections such as: **Gout, Asbestos**, Silica, Amyloid beta (Alzheimer's), Islet amyloid polypetide (T2 diabetes), Hemozoin (Malaria)
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_NALP3 Inflammasome_ * Sensor of damage and cellular stress * Crystals can form and are taken up by cells - this then drives activation and formation of the NALP3 inflammasome * Conditions/Diseases/Infections such as: Gout, Asbestos, Silica, Amyloid beta (...), Islet amyloid polypetide (... diabetes), Hemozoin (Malaria)
* Sensor of damage and cellular stress * Crystals can form and are taken up by cells - this then drives activation and formation of the NALP3 inflammasome * Conditions/Diseases/Infections such as: Gout, Asbestos, Silica, Amyloid beta (**Alzheimer's**), Islet amyloid polypetide (**T2** diabetes), Hemozoin (Malaria)
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_NALP3 Inflammasome_ * Sensor of damage and cellular stress * Crystals can form and are taken up by cells - this then drives activation and formation of the NALP3 inflammasome * Conditions/Diseases/Infections such as: Gout, Asbestos, Silica, Amyloid beta (Alzheimer's), Islet amyloid polypetide (T2 diabetes), Hemozoin (M...)
* Sensor of damage and cellular stress * Crystals can form and are taken up by cells - this then drives activation and formation of the NALP3 inflammasome * Conditions/Diseases/Infections such as: Gout, Asbestos, Silica, Amyloid beta (Alzheimer's), Islet amyloid polypetide (T2 diabetes), Hemozoin (**Malaria**)
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_Frustrated phagocytosis_ * ... hip - fragments break off after grinding over years * ... by a macrophage - gets stuck in the process and puts cell under stress, leading to inflammasome activation and production of IL-1 and IL-18 * These people get inflamed hip, revision and tissue removed
* **Artificial** hip - fragments break off after grinding over years * **Phagocytosed** by a macrophage - gets stuck in the process and puts cell under stress, leading to inflammasome activation and production of IL-1 and IL-18 * These people get inflamed hip, revision and tissue removed
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_Frustrated phagocytosis_ * Artificial hip - fragments break off after grinding over years * Phagocytosed by a macrophage - gets stuck in the process and puts cell under stress, leading to inflammasome activation and production of IL-.. and IL-.. * These people get inflamed hip, revision and tissue removed
* Artificial hip - fragments break off after grinding over years * Phagocytosed by a macrophage - gets stuck in the process and puts cell under stress, leading to inflammasome activation and production of **IL-1 and IL-18** * These people get inflamed hip, revision and tissue removed
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_Inflammasome cleavage of pro-IL-1 and pro-IL-18_ * Activation of either IL-1 receptor family or toll-receptors - driving transcription and translation of IL-1B - made as pro-IL-1B - cleaved by ...-1 released from inflammasome complex - makes mature active form of IL-1B * Same process for IL-18 (requires cleavage by NALP3 inflammasome)
* Activation of either IL-1 receptor family or toll-receptors - driving transcription and translation of IL-1B - made as pro-IL-1B - cleaved by **caspase**-1 released from inflammasome complex - makes mature active form of IL-1B * Same process for IL-18 (requires cleavage by NALP3 inflammasome)
150
_Inflammasome cleavage of pro-IL-1 and pro-IL-18_ * Activation of either IL-1 receptor family or toll-receptors - driving transcription and translation of IL-1B - made as pro-IL-1B - cleaved by caspase-1 released from inflammasome complex - makes mature ... form of IL-1B * Same process for IL-18 (requires cleavage by NALP3 inflammasome)
* Activation of either IL-1 receptor family or toll-receptors - driving transcription and translation of IL-1B - made as pro-IL-1B - cleaved by caspase-1 released from inflammasome complex - makes mature **active** form of IL-1B * Same process for IL-18 (requires cleavage by NALP3 inflammasome)
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_Inflammasome cleavage of pro-IL-1 and pro-IL-18_ * Activation of either IL-1 receptor family or toll-receptors - driving transcription and translation of IL-1B - made as pro-IL-1B - cleaved by caspase-1 released from inflammasome complex - makes mature active form of IL-1B * Same process for IL-... (requires cleavage by NALP3 inflammasome)
* Activation of either IL-1 receptor family or toll-receptors - driving transcription and translation of IL-1B - made as pro-IL-1B - cleaved by caspase-1 released from inflammasome complex - makes mature active form of IL-1B * Same process for **IL-18** (requires cleavage by NALP3 inflammasome)
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_Inflammasome cleavage of pro-IL-1 and pro-IL-18_ * Activation of either IL-1 receptor family or toll-receptors - driving transcription and translation of IL-1B - made as pro-IL-1B - cleaved by ...-1 released from inflammasome complex - makes mature active form of IL-1B * Same process for IL-18 (requires cleavage by NALP3 inflammasome)
* Activation of either IL-1 receptor family or toll-receptors - driving transcription and translation of IL-1B - made as pro-IL-1B - cleaved by **caspase**-1 released from inflammasome complex - makes mature active form of IL-1B * Same process for IL-18 (requires cleavage by NALP3 inflammasome)
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_Gain of function mutations in NLRP3_ * Cryopyrin-Associated Periodic Syndromes (...) - Caused by rare mutations in exon 3 of NLRP3 gene causing over production of IL-1 * 2 - Muckle wells syndrome (Prevalence unknown) and Familial cold autoinflammatory syndrome (1: 1000000)
* Cryopyrin-Associated Periodic Syndromes (**CAPS**) - Caused by rare mutations in exon 3 of NLRP3 gene causing over production of IL-1 * 2 - Muckle wells syndrome (Prevalence unknown) and Familial cold autoinflammatory syndrome (1: 1000000)
154
_Gain of function mutations in NLRP3_ * Cryopyrin-Associated Periodic Syndromes (CAPS) - Caused by rare mutations in exon 3 of NLRP3 gene causing over production of IL-... * 2 - Muckle wells syndrome (Prevalence unknown) and Familial cold autoinflammatory syndrome (1: 1000000)
* Cryopyrin-Associated Periodic Syndromes (CAPS) - Caused by rare mutations in exon 3 of NLRP3 gene causing over production of **IL-1** * 2 - Muckle wells syndrome (Prevalence unknown) and Familial cold autoinflammatory syndrome (1: 1000000)
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_Gain of function mutations in NLRP3_ * Cryopyrin-Associated Periodic Syndromes (CAPS) - Caused by rare mutations in exon 3 of NLRP3 gene causing over production of IL-1 * 2 - ... ... syndrome (Prevalence unknown) and Familial cold autoinflammatory syndrome (1: 1000000)
* Cryopyrin-Associated Periodic Syndromes (CAPS) - Caused by rare mutations in exon 3 of NLRP3 gene causing over production of IL-1 * 2 - **Muckle wells** syndrome (Prevalence unknown) and Familial cold autoinflammatory syndrome (1: 1000000)
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_Gain of function mutations in NLRP3_ * Cryopyrin-Associated Periodic Syndromes (CAPS) - Caused by rare mutations in exon 3 of NLRP3 gene causing over production of IL-1 * 2 - Muckle wells syndrome (Prevalence unknown) and ... ... autoinflammatory syndrome (1: 1000000)
* Cryopyrin-Associated Periodic Syndromes (CAPS) - Caused by rare mutations in exon 3 of NLRP3 gene causing over production of IL-1 * 2 - Muckle wells syndrome (Prevalence unknown) and **Familial cold** autoinflammatory syndrome (1: 1000000)
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_Muckle wells syndrome (Prevalence unknown)_ * Can occur spontaneously or be triggered by ..., ..., fatigue, or other stresses. * Symptoms of fever, rash, arthralgia, conjunctivitis, uveitis, sensorineural deafness, and potentially life-threatening amyloidosis * (Abnormal deposits of a protein called amyloid (amyloidosis) cause progressive kidney damage in about one-third of people with Muckle-Wells syndrome; ) * Can be treated with Anakinra (IL-1RA)
* Can occur spontaneously or be triggered by **cold, heat**, fatigue, or other stresses. * Symptoms of fever, rash, arthralgia, conjunctivitis, uveitis, sensorineural deafness, and potentially life-threatening amyloidosis * (Abnormal deposits of a protein called amyloid (amyloidosis) cause progressive kidney damage in about one-third of people with Muckle-Wells syndrome; ) * Can be treated with Anakinra (IL-1RA)
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_Muckle wells syndrome (Prevalence unknown)_ * Can occur spontaneously or be triggered by cold, heat, fatigue, or other stresses. * Symptoms of fever, rash, arthralgia, conjunctivitis, uveitis, sensorineural deafness, and potentially life-threatening ... * Can be treated with Anakinra (IL-1RA)
* Can occur spontaneously or be triggered by cold, heat, fatigue, or other stresses. * Symptoms of fever, rash, arthralgia, conjunctivitis, uveitis, sensorineural deafness, and potentially life-threatening **amyloidosis** * (Abnormal deposits of a protein called amyloid (amyloidosis) cause progressive kidney damage in about one-third of people with Muckle-Wells syndrome; )
159
_Familial cold autoinflammatory syndrome (1: 1000000)_ * Triggered by exposure to ... * Symptoms of fever urticarial rash with headache, arthralgia, and sometimes conjunctivitis * Can be treated with Anakinra (IL-1RA)
* Triggered by exposure to **cold** * Symptoms of fever urticarial rash with headache, arthralgia, and sometimes conjunctivitis * Can be treated with Anakinra (IL-1RA)
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_Familial cold autoinflammatory syndrome (1: 1000000)_ * Triggered by exposure to cold * Symptoms of ... urticarial rash with headache, arthralgia, and sometimes conjunctivitis * Can be treated with ... (IL-1RA)
* Triggered by exposure to cold * Symptoms of **fever** urticarial rash with headache, arthralgia, and sometimes conjunctivitis * Can be treated with **Anakinra** (IL-1RA)
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_Muckle wells syndrome (Prevalence unknown)_ * Can occur spontaneously or be triggered by cold, heat, fatigue, or other stresses. * Symptoms of fever, rash, arthralgia, conjunctivitis, uveitis, sensorineural deafness, and potentially life-threatening ... * Can be treated with ... (IL-1RA)
* Can occur spontaneously or be triggered by cold, heat, fatigue, or other stresses. * Symptoms of fever, rash, arthralgia, conjunctivitis, uveitis, sensorineural deafness, and potentially life-threatening **amyloidosis** * (Abnormal deposits of a protein called amyloid (amyloidosis) cause progressive kidney damage in about one-third of people with Muckle-Wells syndrome; ) * Can be treated with **Anakinra** (IL-1RA)
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Both Muckle wells syndrome and Familial cold autoinflammatory syndrome can be treated with ... (IL-1RA)
Both Muckle wells syndrome and Familial cold autoinflammatory syndrome can be treated with **Anakinra** (IL-1RA) *(Both are Cryopyrin-Associated Periodic Syndromes (CAPS) - Caused by rare mutations in exon 3 of NLRP3 gene causing over production of IL-1)*
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Both Muckle wells syndrome and Familial cold autoinflammatory syndrome can be treated with **Anakinra (IL-...)**
Both Muckle wells syndrome and Familial cold autoinflammatory syndrome can be treated with **Anakinra (IL-1RA)** *(Both are Cryopyrin-Associated Periodic Syndromes (CAPS) - Caused by rare mutations in exon 3 of NLRP3 gene causing over production of IL-1)*
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_RIG-I-like receptors (RLRs)_ * RIG-I and MDA5 are sensors of cytoplasmic ..., a replication intermediate for viruses. They signal to induce pro-inflammatory ... and IFN.
* RIG-I and MDA5 are sensors of cytoplasmic **RNA**, a replication intermediate for viruses. They signal to induce pro-inflammatory **cytokines** and IFN. * RIG-I - Binds to single stranded RNA containing 5’-triphosphate (our 5’ RNA is capped so not recognised) * MDA5 - Preferentially recognizes long double stranded RNA, Critical for picornavirus detection, Mutations are rare but have been associated with IFN related diseases, e.g. systemic lupus erythematosus and Aicardi–Goutières syndrome.
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_RIG-I-like receptors (RLRs)_ * RIG-I and MDA5 are sensors of cytoplasmic RNA, a replication intermediate for viruses. They signal to induce pro-inflammatory cytokines and IFN. * RIG-I - Binds to ... stranded RNA containing 5’-triphosphate (our 5’ RNA is capped so not recognised) * MDA5 - Preferentially recognizes long ... stranded RNA, Critical for picornavirus detection, Mutations are rare but have been associated with IFN related diseases, e.g. systemic lupus erythematosus and Aicardi–Goutières syndrome.
* RIG-I and MDA5 are sensors of cytoplasmic RNA, a replication intermediate for viruses. They signal to induce pro-inflammatory cytokines and IFN. * RIG-I - Binds to **single** stranded RNA containing 5’-triphosphate (our 5’ RNA is capped so not recognised) * MDA5 - Preferentially recognizes long **double** stranded RNA, Critical for picornavirus detection, Mutations are rare but have been associated with IFN related diseases, e.g. systemic lupus erythematosus and Aicardi–Goutières syndrome.
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_RIG-I_ * RIG-I and MDA5 are sensors of ... ..., a replication intermediate for viruses. They signal to induce pro-inflammatory cytokines and IFN. * RIG-I Binds to ... stranded RNA containing 5’-triphosphate (our 5’ RNA is capped so not recognised)
* RIG-I and MDA5 are sensors of **cytoplasmic** **RNA**, a replication intermediate for viruses. They signal to induce pro-inflammatory cytokines and IFN. * RIG-I Binds to **single** stranded RNA containing 5’-triphosphate (our 5’ RNA is capped so not recognised)
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_MDA5_ * RIG-I and MDA5 are sensors of cytoplasmic RNA, a replication intermediate for viruses. They signal to induce pro-inflammatory cytokines and IFN. * Preferentially recognizes long ... stranded RNA * Critical for ... detection * Mutations are rare but have been associated with IFN related diseases, e.g. systemic lupus erythematosus and Aicardi–Goutières syndrome.
* RIG-I and MDA5 are sensors of cytoplasmic RNA, a replication intermediate for viruses. They signal to induce pro-inflammatory cytokines and IFN. * Preferentially recognizes long **double** stranded RNA * Critical for **picornavirus** detection * Mutations are rare but have been associated with IFN related diseases, e.g. systemic lupus erythematosus and Aicardi–Goutières syndrome.
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_MDA5_ * RIG-I and MDA5 are sensors of cytoplasmic RNA, a replication intermediate for viruses. They signal to induce pro-inflammatory cytokines and IFN. * Preferentially recognizes long ... stranded RNA * Critical for ... detection * Mutations are rare but have been associated with IFN related diseases, e.g. systemic ... erythematosus and Aicardi–... syndrome.
* RIG-I and MDA5 are sensors of cytoplasmic RNA, a replication intermediate for viruses. They signal to induce pro-inflammatory cytokines and IFN. * Preferentially recognizes long **double** stranded RNA * Critical for **picornavirus** detection * Mutations are rare but have been associated with IFN related diseases, e.g. systemic **lupus** erythematosus and Aicardi–**Goutières** syndrome.
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_Cytosolic DNA sensors_ * Stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy (SAVI) is an autoinflammatory disease caused by ...-of-function mutations in the gene that codes for STING. Patients produce too much type 1 IFN causing abnormal inflammation throughout the body, especially in the skin, blood vessels, and lungs.
* Stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy (SAVI) is an autoinflammatory disease caused by **gain**-of-function mutations in the gene that codes for STING. Patients produce too much type 1 IFN causing abnormal inflammation throughout the body, especially in the skin, blood vessels, and lungs.
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_Cytosolic DNA sensors_ * Stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy (SAVI) is an autoinflammatory disease caused by gain-of-function mutations in the gene that codes for STING. Patients produce too much type 1 ... causing abnormal inflammation throughout the body, especially in the skin, blood vessels, and lungs.
* Stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy (SAVI) is an autoinflammatory disease caused by gain-of-function mutations in the gene that codes for STING. Patients produce too much type 1 **IFN** causing abnormal inflammation throughout the body, especially in the skin, blood vessels, and lungs.
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_Cytosolic DNA sensors_ * Stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy (SAVI) is an autoinflammatory disease caused by gain-of-function mutations in the gene that codes for STING. Patients produce too much type ... IFN causing abnormal inflammation throughout the body, especially in the skin, blood vessels, and lungs.
* Stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy (SAVI) is an autoinflammatory disease caused by gain-of-function mutations in the gene that codes for STING. Patients produce too much **type 1 IFN** causing abnormal inflammation throughout the body, especially in the skin, blood vessels, and lungs.
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_Cytosolic DNA sensors_ * Stimulator of interferon genes (...)-associated vasculopathy with onset in infancy (SAVI) is an autoinflammatory disease caused by gain-of-function mutations in the gene that codes for .... Patients produce too much type 1 IFN causing abnormal inflammation throughout the body, especially in the skin, blood vessels, and lungs.
* Stimulator of interferon genes (**STING**)-associated vasculopathy with onset in infancy (SAVI) is an autoinflammatory disease caused by gain-of-function mutations in the gene that codes for **STING**. Patients produce too much type 1 IFN causing abnormal inflammation throughout the body, especially in the skin, blood vessels, and lungs.
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Stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy (SAVI) is an autoinflammatory disease caused by ...-of-function mutations in the gene that codes for STING
Stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy (SAVI) is an autoinflammatory disease caused by **gain**-of-function mutations in the gene that codes for STING
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_Acute Phase Response_ * Acute phase proteins are mainly produced by the ... * Induced by cytokines such as TNF, IL-6 and IL-1 during infection and inflammation * Acute phase proteins can activate complement and induce opsonisation/phagocytosis * Raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are characteristic of an acute phase response and are used clinically to detect inflammation
* Acute phase proteins are mainly produced by the **liver** * Induced by cytokines such as TNF, IL-6 and IL-1 during infection and inflammation * Acute phase proteins can activate complement and induce opsonisation/phagocytosis * Raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are characteristic of an acute phase response and are used clinically to detect inflammation
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_Acute Phase Response_ * Acute phase proteins are mainly produced by the ... * Induced by ... such as TNF, IL-6 and IL-1 during infection and inflammation * Acute phase proteins can activate complement and induce opsonisation/phagocytosis * Raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are characteristic of an acute phase response and are used clinically to detect inflammation
* Acute phase proteins are mainly produced by the **liver** * Induced by **cytokines** such as TNF, IL-6 and IL-1 during infection and inflammation * Acute phase proteins can activate complement and induce opsonisation/phagocytosis * Raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are characteristic of an acute phase response and are used clinically to detect inflammation
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_Acute Phase Response_ * Acute phase proteins are mainly produced by the ... * Induced by cytokines such as TNF, IL-6 and IL-1 during infection and inflammation * Acute phase proteins can activate ... and induce opsonisation/phagocytosis * Raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are characteristic of an acute phase response and are used clinically to detect inflammation
* Acute phase proteins are mainly produced by the **liver** * Induced by cytokines such as TNF, IL-6 and IL-1 during infection and inflammation * Acute phase proteins can activate **complement** and induce opsonisation/phagocytosis * Raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are characteristic of an acute phase response and are used clinically to detect inflammation
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_Acute Phase Response_ * Acute phase proteins are mainly produced by the liver * Induced by cytokines such as ..., IL-6 and IL-1 during infection and inflammation * Acute phase proteins can activate complement and induce opsonisation/phagocytosis * Raised ... sedimentation rate (...) and C-reactive protein (CRP) are characteristic of an acute phase response and are used clinically to detect inflammation
* Acute phase proteins are mainly produced by the liver * Induced by cytokines such as **TNF**, IL-6 and IL-1 during infection and inflammation * Acute phase proteins can activate complement and induce opsonisation/phagocytosis * Raised erythrocyte sedimentation rate (**ESR**) and C-reactive protein (CRP) are characteristic of an acute phase response and are used clinically to detect inflammation
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_Acute Phase Response_ * Acute phase proteins are mainly produced by the liver * Induced by cytokines such as TNF, IL-.. and IL-.. during infection and inflammation * Acute phase proteins can activate complement and induce .../... * Raised erythrocyte sedimentation rate (ESR) and C-... protein (...) are characteristic of an acute phase response and are used clinically to detect inflammation
* Acute phase proteins are mainly produced by the liver * Induced by cytokines such as TNF, **IL-6 and IL-1** during infection and inflammation * Acute phase proteins can activate complement and induce **opsonisation**/**phagocytosis** * Raised erythrocyte sedimentation rate (ESR) and C-**reactive** protein (**CRP**) are characteristic of an acute phase response and are used clinically to detect inflammation
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Acute phase proteins can activate ... and induce opsonisation/phagocytosis
Acute phase proteins can activate **complement** and induce opsonisation/phagocytosis
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Raised ... ... rate (...) and ...-... protein (...) are characteristic of an acute phase response and are used clinically to detect inflammation
**Raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)** are characteristic of an acute phase response and are used clinically to detect inflammation
181
Raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are characteristic of an ... ... response and are used clinically to detect inflammation
Raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are characteristic of an **acute phase** response and are used clinically to detect inflammation
182
Raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are characteristic of an acute phase response and are used clinically to detect ...
Raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are characteristic of an acute phase response and are used clinically to detect **inflammation**
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... increases as serum becomes more viscous due to the presence of extra protein.
**ESR** increases as serum becomes more viscous due to the presence of extra protein.

Year 2 Medicine (162 decks)

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