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Immunology > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

How does innate immunity differ from adaptive immunity?

A

Innate immunity is non-specific and fast whereas adaptive immunity is more specific to a certain type of pathogen and is slower

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2
Q

What are the physical barriers of the body to pathogens?

A

Things such as hair, wax, tears, mucus, membranes, air movement, etc

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3
Q

What are barrier defenses in the body?

A

Barrier defenses are part of the body’s most basic defense mechanisms. They don’t respond to infection but are continuously working to protect against a broad range of pathogens

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4
Q

What are the types of barrier defenses?

A
  • Flow of air or fluid -reduces the chance of pathogen attaching
  • Antimicrobial enzymes (lysozyme in tears)
  • Low pH
  • Defensins- antimicrobial peptides disrupt cell membranes and virus envelopes
  • Normal flora- outcompete pathogens
  • Ciliated and goblet cells
  • Epithelial tight junctions-restrict movement of pathogens
  • Tissue-resident immune cells- engulf and kill pathogens
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5
Q

What is the role of ciliated cells as a barrier defense to infection?

A

Move mucus along to flush out pathogens

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6
Q

What is the role of goblet cells as a barrier defense to infection?

A

Produce mucus which acts as a sticky barrier

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7
Q

What is inflammation?

A

The body’s response to damage

-progressed through a series of stages until it is resolved and tissue returns to normal

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8
Q

What are the cardinal signs of inflammation?

A 
Rubor-redness
Calor-heat
Tumor-swelling
Dolor-pain
Functio laesa-loss of function
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9
Q

What is the role of histamine in inflammation?

A

Secreted by mast cells, basophils and platelets
Binds to histamine receptors which leads to:
-vasodilation for increased blow flow
-Exudation of fluid from blood into tissues

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10
Q

How can inflammation occur without infection?

A

Due to tissue damage

  • fragments of a cell are released through damage
  • these contain DAMPs which bind to recpetors which induce imflammatory cytokine release and trigger inflammation
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11
Q

What are DAMPs and what do they bind to?

A

DAMPs- Damage Associated Molecular Patterns

-bind to Pattern Recognition Receptors (PRR)

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12
Q

What are PAMPs and what do they they bind to?

A

PAMPs- Pattern Associated Molecular Patterns

-bind to Pattern Recognition Receptors (PRR)

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13
Q

How do cells detect and find pathogens?

A

They realese DAMPs and PAMPs which bind to Pattern Recognition Receptors (PRR). This activates cells to talk to each other and kill the pathogen

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14
Q

What are the different types of Pattern Recognition Receptors (PRRs)?

A

External : Toll like receptors
Phagocytic receptors-induce uptake of pathogen into endosomes (killing of pathogen)
Internal: Toll like receptors
NOD and RIG like receptors

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15
Q

What are the Toll like receptors on the plasma membrane?

A

TLR 4
TLR5
TLR2 and TLR 1/6

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16
Q

What binds to TLR 4?

A

LPS (lipopolysaccharides)

- also known as endotoxins bind to this. Found in the outer membrane of gram-negative bacteria

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17
Q

What binds to TLR 5?

A

Flagellin

- a globular protein found in the flagellum of bacteria

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18
Q

What binds to TLR 2 and TLR 1/6?

A

Lipoproteins

- lipoproteins are in the cell wall of gram positive and negative bacteria

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19
Q

What are the internal Toll like receptors (endosomal) ?

A

TLR 3
TLR 7
TLR 8
TLR 9

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20
Q

What binds to TLR 3?

A

Double stranded RNA

-a form of genetic info carried by some viruses

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21
Q

What binds to TLR 7?

A

Single stranded RNA ( Guanine rich)

-a form of genetic info carried by some viruses

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22
Q

What binds to TLR 8?

A

Single stranded RNA ( Guanine and Uracil rich)

-a form of genetic info carried by some viruses

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23
Q

What binds to TLR 9?

A

Unmethylated bacteria CpG DNA

-regions of DNA where cytosine nucleotide is followed by a guanine nucleotide

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24
Q

How do immune cells communicate between each other?

A

Through cell to cell contact

Release of cytokines

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25
Q

What are the 2 main classes of cytokines?

A

Proinflammatory cytokines

Anti-inflammatory cytokines

26
Q

What are proinflammatory cytokines?

A

Tell cells there is danger and to turn on inflammation

(e.g TNFa, IL-6)

27
Q

What are anti-inflammatory cytokines?

A

Tells cells there is no danger, keeps cells inactive and turns off inflammation

28
Q

What are the effects of pro-inflammatory cytokines?

A

Triggers inflammation

-tight junctions between cells open which allows the movement of fluid out and neutrophils in

29
Q

What is a phagoctye?

A

A cell that injests microbes by phagocytosis or pinocytosis.

30
Q

What is a macrophage?

A

A type of phagoctye

- live in the tissue and are activated by pathogens to make cytokins to attract other cells

31
Q

How do macrophages kill the pathogen?

A

Pathogen recognised by PRR which activated phagocytosis

  • pathogen internalised in a phagocytic vacuole, which fuses with a lysosome containing antimicrobial peptides, enzymes and reactive oxygen species
  • activated macrophages make pro-inflammatory cytoines to attract other cells
  • pathogen killed by oxidative burst and digested by enzymes
32
Q

How do immune cells find the pathogen?

A

When inflammed tissues or cells proudce inflammatory cytokines, chemokines produced
-immune cells move to where the chemokine concentration is the highest
(Neutraphils arrive first, triggering phagocytosis, apoptosis and netosis)

33
Q

What is the effect of alot of inflammation?

A

Continued release of pro-inflammatory cytokines can be damaging

  • damaged blood vessels produce bradykinin which increase vascular permeability and cause pain
  • can lead to chronic inflammation
34
Q

How do other cells recognise intracellular microbes?

A

Infected cells hold up flags (present the pathogen’s antigen on cell surface) to show they are infected and should be killed

35
Q

How does a cell recognise an intracellular pathogen and what response does it have?

A

The pathogen recognised by intracellular toll like recpetors
-the receptors release interferon response factors (IRF) which bind to DNA and act as a transcription factor to produce Type 1 interferons ( IFNa and IFNb) which increase viral defences

36
Q

What are the different types of type 1 interferons?

A

IFNa and IFNb

37
Q

What are the anti-viral responses type 1 interferons cause?

A

Prevent virus from replicating:
-IFNa and IFNb bind to IFN receptor which activates genes that degrade viral DNA and halt protein synthesis needed to make viral capsules
Sacrifice infected cells:
-Natural killer (NK) cells kill virus infected cells by apoptosis

38
Q

How do Natural killer cells know which cells to kill when non are foreign?

A

Healthy cells have a higher ratio of inhibitory ligands on cell membrane- no NK cell activation
Cancer/infected cells have a higher ratio of activating ligands on cell membrane- NK cell activation

39
Q

How do Natural Killer cells destroy cells?

A

Once the cell is recognised as non-self they realease granules containing perforin and granzyme
-perforin punches a hole in the cell and granzyme enters and breaks down the cell

40
Q

What happens if the pathogen is not cleared using innate immunity?

A

Crosses over from innate to adaptive immunity

-signalled by dendritic cells

41
Q

What is the complement pathway and when does it occur?

A
  • Happens instantly when epithelial barriers are breached
  • It is an ezyme cascade that helps phagocytic cells clear microbes, promote inflammation and attack a pathogens cell membrane
42
Q

What are the 3 different complement pathways?

A

Classical pathway
Lectin pathway
Alternative pathway

43
Q

What triggers the classical pathway of the complement system?

A

Activated by the antigen-antibody complex that binds to the C1 complex

44
Q

Describe the classical pathway of the complement pathway?

A
  • C1 complex activated by antigen-antibody complex
  • Activated C1 complex cleaves C4 and C2
  • C4b and C2b join to from C3-convertase which cleaves C3
  • C3b binds to the C3-convertase to form C5-convertase
  • C5-convertase cleaves C5
  • C5b recruits C6,7,8,9 to form the membrane attack complex (C5b-9)
45
Q

What triggers the alternative pathway of the complement system?

A

The spontaneous hydrolysis of C3. The pathway is triggered when C3b binds directly to a microbe

46
Q

Describe the alternative pathway in the complement system?

A
  • C3 spontaneously hydrolyses
  • Factor D cleaves factor B in Bb and Ba
  • C3b combines with Bb to form C3 convertase
  • C3 convertase cleaves C3
  • C3b combines with C3 convertase to form C5 convertase
  • C5-convertase cleaves C5
  • C5b recruits C6,7,8,9 to form the membrane attack complex (C5b-9)
47
Q

What triggers the lectin pathway of the complement pathway?

A

Triggered by pathogen membranes containing mannose. Mannose-binding-lectin binds to the mannose and allowing MASP1 and 2 to bind
-creates a C1 like complex which initiates pathway the same as classical pathway

48
Q

Describe the lectin pathway of the complement pathway?

A
  • Mannose-binding lectin bind to mannose on pathogen membrane
  • MASP1 and 2 bind to form a C1 like complex
  • C1 like complex cleaves C4 and C2
  • C4b and C2b join to from C3-convertase which cleaves C3
  • C3b binds to the C3-convertase to form C5-convertase
  • C5-convertase cleaves C5
  • C5b recruits C6,7,8,9 to form the membrane attack complex (C5b-9)
49
Q

How does the complement pathway trigger opsonization?

A

Pathogen are covered in the C3b protein. Phagoctyes recognise the C3b through complement receptors and kill the pathogen

50
Q

What is chemotaxis?

A

Chemotaxis is the process by which phagocytes follow the cytokine ‘scent’ to the infected area which they increase in number

51
Q

How does the complement pathway cause chemotaxis?

A

C3a and C5a recruit phagocytic cells and promote inflammation

52
Q

What are acute phase proteins?

A 
A class of proteins released by the liver in response to inflammation
-such as mannose binding lectin, fibrinogen (a clotting factor)
53
Q

What are some examples of acute phase proteins?

A 
SP-A
SP-D
Mannose-binding-lectin
Fibrinogen
C-reactive protein
Serum amyloid protein
54
Q

What is the function of SP-A and SP-B?

A

Are acute phase proteins secreted by the liver in response to inflammation
-they act as opsonins (marks an antigen to improve phagocytosis)

55
Q

What is the function of fibrinogen?

A

Is an acute phase proteins secreted by the liver in response to inflammation
-Acts as a clotting factor

56
Q

What is the function of C-reactive protein?

A

Is an acute phase proteins secreted by the liver in response to inflammation
-assists in complement binding to foreign and damaged cells, and acts as an opsonin

57
Q

What is the function of neurophils?

A

A type of white blood cell. They are the first responders to invading microbes, killing invading microbes by phagocytosis ( a type of phagocyte)

58
Q

What is the function of eosinophils?

A

A type of white blood cell. They are major effector cells. They aid with the killing of cells by phagocytosis, and also promote inflammation.

59
Q

What is the function of basophils?

A

Type of white blood cell. Basophils are recruited to sites of inflammation and they can be activated by a variety of PAMPs. When stimulated basophils release their granule contents including histamine, IL-4 and IL-13

60
Q

What is the function of monocytes?

A

Type of white blood cell that circulate in blood and spleen.

61
Q

What is the function of macrophages?

A

Specialised cells that originate from monocytes. Involved in the phagocytosis of bacteria and other harmful organisms. They also present antigens to T cells using MHC II. They release cytokines IL-1, IL-6 and TNFa

62
Q

What is the function of mast cells?

A

Long lived tissue resisdent cells that play an important role in inflammation. Activated by the Fc region of the IgE immunoglobulin binding to the mast cell. The mast cell then releases histamine and other inflammatory mediators

Immunology (10 decks)

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