An Overview of Immunology Flashcards
(84 cards)
1
Q
What is an antigen?
A
Anything the immune system responds to
2
Q
Antigens are usually …
A
protein
3
Q
Antigens are not necessarily ‘…’
A
‘bad’
4
Q
The main role of the immune system is to protect from …
A
infection
5
Q
What is an antigen receptor?
A
Recognises the antigen -> fundamental basis of immunity, basis of division into innate and adaptive
6
Q
The innate immune system fundamentally recognizes antigens using ….
A
Germline-encoded pattern-recognition receptors
7
Q
The adaptive immune system is activated in the presence of pathogens - … cells and … cells recognise antigens through …-specific … and … cell receptors
A
The adaptive immune system is activated in the presence of pathogens - T cells and B cells recognise antigens through antigen-specific T and B cell receptors
8
Q
… mechanisms are an action to respond to the antigen (innate and adaptive have a lot of shared mechanisms - distinction is in the way they recognise the antigen rather than what happens next)
A
effector mechanisms
9
Q
The cells of the immune system originate in the … …
A
The cells of the immune system originate in the bone marrow
10
Q
Pluripotent hematopoietic stem cells thus differentiate into bone marrow as … or … stem cells.
A
Pluripotent hematopoietic stem cells thus differentiate into bone marrow as myeloid or lymphoid stem cells.
11
Q
Pluripotent hematopoietic stem cells thus differentiate into bone marrow as lymphoid or myeloid stem cells (common lymphoid progenitor or common myeloid progenitor). These then give rise to the two lineages of immunological cell. We have lymphocyte lineage (… cells) and myeloid lineage (cells such as …)
A
Pluripotent hematopoietic stem cells thus differentiate into bone marrow as lymphoid or myeloid stem cells (common lymphoid progenitor or common myeloid progenitor). These then give rise to the two lineages of immunological cell. We have lymphocyte lineage (T,B, NK cells) and myeloid lineage (cells such as neutrophils, eosinphil, basophil, monocyte, mast cell)
12
Q
Pluripotent hematopoietic stem cells thus differentiate into bone marrow as … or … stem cells.
A
Pluripotent hematopoietic stem cells thus differentiate into bone marrow as myeloid or lymphoid stem cells.
13
Q
Pluripotent hematopoietic stem cells thus differentiate into bone marrow as lymphoid or myeloid stem cells (common lymphoid progenitor or common myeloid progenitor). These then give rise to the two lineages of immunological cell. We have lymphocyte lineage (… cells) and myeloid lineage (cells such as …)
A
Pluripotent hematopoietic stem cells thus differentiate into bone marrow as lymphoid or myeloid stem cells (common lymphoid progenitor or common myeloid progenitor). These then give rise to the two lineages of immunological cell. We have lymphocyte lineage (T,B, NK cells) and myeloid lineage (cells such as neutrophils, eosinphil, basophil, monocyte, mast cell)
14
Q
What is the function of a neutrophil?
A
Phagocytosis
15
Q
What cell is this? (White blood cell)
A
Neutrophil
16
Q
What cell is this? (White blood cell)
A
Neutrophil
17
Q
What is the function of an eosinophil? (is not fully understood - may be important in what infections?)
A
? Helminth (parasitic) infection, allergies also
18
Q
What cell is this? (White blood cell)
A
Eosinophil
19
Q
What cell is this? (White blood cell)
A
Monocyte (Circulating) Called Macrophage (in the tissue)
20
Q
What is the function of a monocyte? (called macrophage in tissue)
A
Phagocytosis, Antigen presentation
21
Q
What is the function of a dendritic cell?
A
Antigen presentation
22
Q
What cell is this?
A
Dendritic cell
23
Q
What cell is this? (White blood cell)
A
Basophil - tissue-resident counterpart = mast cell
24
Q
What is the function of a basophil? (tissue-resident counterpart = mast cell)
A
?Helminth (parasitic infection) also in allergy - release histamine
25
_Lymphoid lineage_
* Similar size to ...
* Little ... with few ...
* ... cells - make antibody, antigen presentation
* ... cells - ... (help other components of immunity) ... (kill infected cells)
* T and B cells = ... immunity
* NK cells are actually ... lymphocytes. Direct lysis of infected cells and antibody-dependent cellular cytotoxicity
* Similar size to **RBC**
* Little **cytoplasm** with few **granules**
* **B** cells - make antibody, antigen presentation
* **T** cells - **CD4** (help other components of immunity) **CD8** (kill infected cells)
* T and B cells = **adaptive** immunity
* NK cells are actually **innate** lymphocytes. Direct lysis of infected cells and antibody-dependent cellular cytotoxicity
26
_Lymphoid lineage_
* Similar size to ...
* Little ... with few ...
* ... cells - make antibody, antigen presentation
* ... cells - ... (help other components of immunity) ... (kill infected cells)
* T and B cells = ... immunity
* NK cells are actually ... lymphocytes. Direct lysis of infected cells and antibody-dependent cellular cytotoxicity
* Similar size to **RBC**
* Little **cytoplasm** with few **granules**
* **B** cells - make antibody, antigen presentation
* **T** cells - **CD4** (help other components of immunity) **CD8** (kill infected cells)
* T and B cells = **adaptive** immunity
* NK cells are actually **innate** lymphocytes. Direct lysis of infected cells and antibody-dependent cellular cytotoxicity
27
Only T cells do not mature in the bone marrow, they mature in the ...
thymus
28
_Communication - Intercellular Signalling_
* What types are there?
* Endocrine - hormones released to act on a target cell
* Paracrine - nearby cells
* Autocrine - acts on own cell
* Juxtacrine - direct contact with another cell
29
_Communication - Intercellular Signalling_
* What types are there?
* Endocrine - hormones released to act on a target cell
* Paracrine - nearby cells
* Autocrine - acts on own cell
* Juxtacrine - direct contact with another cell
30
Often, cells that are near one another communicate through the release of chemical messengers (ligands that can diffuse through the space between the cells). This type of signaling, in which cells communicate over relatively short distances, is known as ... signaling.
Often, cells that are near one another communicate through the release of chemical messengers (ligands that can diffuse through the space between the cells). This type of signaling, in which cells communicate over relatively short distances, is known as **paracrine** signaling.
31
In autocrine signalling, the cell targets...
itself
32
_Communication: Cytokines and Chemokines_
* Cytokines are small proteins released by cells that have an effect on another cell - (important for communication between cells of the immune system and between immune system cells and other cells and tissues) - Known as ... then a number referring to order of discovery, but some are named differently eg TGF-B, IFN,g, TNF-a
* Chemokines are similarly defined, but - different structure, receptors and nomenclature and main role is temporal and spatial ... of cells and tissues
* Cytokines are small proteins released by cells that have an effect on another cell - (important for communication between cells of the immune system and between immune system cells and other cells and tissues) - Known as **Interleukin** then a number referring to order of discovery, but some are named differently eg TGF-B, IFN,g, TNF-a
* Chemokines are similarly defined, but - different structure, receptors and nomenclature and main role is temporal and spatial **organisation** of cells and tissues
33
_Communication: Cytokines and Chemokines_
* Cytokines are small ... released by cells that have an effect on ... - (important for communication between cells of the immune system and between immune system cells and other cells and tissues) - Known as Interleukin then a number referring to order of discovery, but some are named differently eg TGF-B, IFN,g, TNF-a
* Chemokines are similarly defined, but - different structure, receptors and nomenclature and main role is ... and ... organisation of cells and tissues
* Cytokines are small **proteins** released by cells that have an effect on **another cell** - (important for communication between cells of the immune system and between immune system cells and other cells and tissues) - Known as Interleukin then a number referring to order of discovery, but some are named differently eg TGF-B, IFN,g, TNF-a
* Chemokines are similarly defined, but - different structure, receptors and nomenclature and main role is **temporal** and **spatial** organisation of cells and tissues
34
_Antigen receptors_
* The receptor that cells use to recognise antigen is a key concept in immunology, and forms the basis of separating two immunological arms: ... and ...
* The receptor that cells use to recognise antigen is a key concept in immunology, and forms the basis of separating two immunological arms: innate and adaptive
35
_Key features of innate antigen receptors_
* Do not recognise antigen ...
* ... recognition receptors (PRRs)
* Recognise 'pathogen associated molecular patterns (...)
* Genome-encoded
* Not clonally distributed
* Do not recognise antigen **specifically**
* **Pattern** recognition receptors (PRRs)
* Recognise 'pathogen associated molecular patterns (**PAMPS**)
* Genome-encoded
* Not clonally distributed
36
_Key features of innate antigen receptors_
* Do not recognise antigen specifically
* Pattern recognition receptors (PRRs)
* Recognise 'pathogen associated molecular patterns (PAMPS)
* ...-encoded
* Not clonally distributed
* Do not recognise antigen specifically
* Pattern recognition receptors (PRRs)
* Recognise 'pathogen associated molecular patterns (PAMPS)
* **Genome**-encoded
* Not clonally distributed
37
_Key features of innate antigen receptors_
* Do not recognise antigen specifically
* Pattern recognition receptors (PRRs)
* Recognise 'pathogen associated molecular patterns (PAMPS)
* Genome-encoded
* Not ... distributed
* Do not recognise antigen specifically
* Pattern recognition receptors (PRRs)
* Recognise 'pathogen associated molecular patterns (PAMPS)
* Genome-encoded
* Not **clonally** distributed
38
_Key features of innate antigen receptors_
* Do not recognise antigen specifically
* Pattern recognition receptors (PRRs)
* Recognise '... ... ... ... (PAMPS)
* Genome-encoded
* Not clonally distributed
* Do not recognise antigen specifically
* Pattern recognition receptors (PRRs)
* Recognise '**pathogen associated molecular patterns** (PAMPS)
* Genome-encoded
* Not clonally distributed
39
_Key features of innate antigen receptors_
* Do not recognise antigen specifically
* Pattern recognition receptors (PRRs)
* Recognise 'pathogen associated molecular patterns (PAMPS)
* ...-encoded
* Not ... distributed
* Do not recognise antigen specifically
* Pattern recognition receptors (PRRs)
* Recognise 'pathogen associated molecular patterns (PAMPS)
* **Genome**-encoded
* Not **clonally** distributed
40
_Key features of innate antigen receptors_
* Do not recognise antigen specifically
* ... ... receptors (...s)
* Recognise 'pathogen associated molecular patterns (PAMPS)
* Genome-encoded
* Not clonally distributed
* Do not recognise antigen specifically
* **Pattern recognition receptors (PRRs)**
* Recognise 'pathogen associated molecular patterns (PAMPS)
* Genome-encoded
* Not clonally distributed
41
_Manose binding ligand (MBL)_
* Example of a ... ... ...
* Recognises mannose and fucose residues with correct spacing - binds to these
* Ones with different spacing not bound by MBL
* Example of a **pattern recognition receptor**
* Recognises mannose and fucose residues with correct spacing - binds to these
* Ones with different spacing not bound by MBL
42
_Manose binding ligand (MBL)_
* Example of a pattern recognition receptor
* Recognises .... and ... residues with correct spacing - binds to these
* Ones with different spacing not bound by MBL
* Example of a pattern recognition receptor
* Recognises **mannose** and **fucose** residues with correct spacing - binds to these
* Ones with different spacing not bound by MBL
43
_Classical features of innate immune receptors/defences (per mod 102)_
* Work ... – ... line of defence
* Adaptive immunity takes more time to be activated
* Unable to ‘learn’, as germline encoded and therefore cannot change – therefore no memory
* All of these statements are still partially valid, but the reality is far more complex – see later lectures for more detail
* Work **quickly** – **first** line of defence
* Adaptive immunity takes more time to be activated
* Unable to ‘learn’, as germline encoded and therefore cannot change – therefore no memory
* All of these statements are still partially valid, but the reality is far more complex – see later lectures for more detail
44
_Classical features of innate immune receptors/defences (per mod 102)_
* Work ... – ... line of defence
* ... immunity takes more time to be activated
* Unable to ‘learn’, as germline encoded and therefore cannot change – therefore no memory
* All of these statements are still partially valid, but the reality is far more complex – see later lectures for more detail
* Work **quickly** – **first** line of defence
* **Adaptive** immunity takes more time to be activated
* Unable to ‘learn’, as germline encoded and therefore cannot change – therefore no memory
* All of these statements are still partially valid, but the reality is far more complex – see later lectures for more detail
45
_Classical features of innate immune receptors/defences (per mod 102)_
* Work ... – ... line of defence
* Adaptive immunity takes more time to be activated
* Unable to ‘...’, as germline encoded and therefore cannot change – therefore no ...
* All of these statements are still partially valid, but the reality is far more complex – see later lectures for more detail
* Work **quickly** – **first** line of defence
* Adaptive immunity takes more time to be activated
* Unable to ‘**learn**’, as germline encoded and therefore cannot change – therefore no **memory**
* All of these statements are still partially valid, but the reality is far more complex – see later lectures for more detail
46
_Key features of adaptive antigen receptors_
* Recognise antigen ...
* T cell receptor, B cell receptor (antibody)
* Produced by random somatic recombination events between gene segments
* Huge receptor diversity
* Clonally distributed
* Permit specificity and memory in immunity
* Recognise antigen **specifically**
* T cell receptor, B cell receptor (antibody)
* Produced by random somatic recombination events between gene segments
* Huge receptor diversity
* Clonally distributed
* Permit specificity and memory in immunity
47
_Key features of adaptive antigen receptors_
* Recognise antigen specifically
* T cell receptor, B cell receptor (antibody)
* Produced by ... ... ... events between gene segments
* Huge receptor diversity
* Clonally distributed
* Permit specificity and memory in immunity
* Recognise antigen specifically
* T cell receptor, B cell receptor (antibody)
* Produced by **random somatic recombination** events between gene segments
* Huge receptor diversity
* Clonally distributed
* Permit specificity and memory in immunity
48
_Key features of adaptive antigen receptors_
* Recognise antigen specifically
* T cell receptor, B cell receptor (antibody)
* Produced by random somatic recombination events between gene segments
* Huge receptor ...
* ... distributed
* Permit specificity and memory in immunity
* Recognise antigen specifically
* T cell receptor, B cell receptor (antibody)
* Produced by random somatic recombination events between gene segments
* Huge receptor **diversity**
* **Clonally** distributed
* Permit specificity and memory in immunity
49
_Key features of adaptive antigen receptors_
* Recognise antigen specifically
* T cell receptor, B cell receptor (antibody)
* Produced by random somatic recombination events between gene segments
* Huge receptor diversity
* Clonally distributed
* Permit ... and ... in immunity
* Recognise antigen specifically
* T cell receptor, B cell receptor (antibody)
* Produced by random somatic recombination events between gene segments
* Huge receptor diversity
* Clonally distributed
* Permit **specificity** and **memory** in immunity
50
_Key features of adaptive antigen receptors_
* Recognise antigen specifically
* T cell receptor, B cell receptor (antibody)
* Produced by random somatic recombination events between gene segments
* Huge receptor diversity
* ... distributed
* Permit ... and memory in immunity
* Recognise antigen specifically
* T cell receptor, B cell receptor (antibody)
* Produced by random somatic recombination events between gene segments
* Huge receptor diversity
* **Clonally** distributed
* Permit **specificity** and memory in immunity
51
_Key features of adaptive antigen receptors_
* Recognise antigen specifically
* ... cell receptor, ... cell receptor (antibody)
* Produced by random somatic recombination events between gene segments
* Huge receptor diversity
* Clonally distributed
* Permit specificity and memory in immunity
* Recognise antigen specifically
* **T** cell receptor, **B** cell receptor (antibody)
* Produced by random somatic recombination events between gene segments
* Huge receptor diversity
* Clonally distributed
* Permit specificity and memory in immunity
52
B cell receptor (antibody) may be ...-bound or ... - it recognises the intact ...
B cell receptor (antibody) may be **surface**-bound or **secreted -** it recognises the intact **antigen**
53
Label the B-cell receptor
54
Label the B-cell receptor
55
Label the B-cell receptor
56
Label the B-cell receptor
57
The T cell receptor is very similar to the B cell receptor but only a ... receptor on CD4 and CD8 T cells - Recognises processed antigen in the form of linear ...
The T cell receptor is very similar to the B cell receptor but only a **surface** receptor on CD4 and CD8 T cells - Recognises processed antigen in the form of linear **peptides**
58
The T cell receptor is very similar to the B cell receptor but only a ... receptor on CD4 and CD8 T cells - Recognises processed antigen in the form of linear ...
The T cell receptor is very similar to the B cell receptor but only a **surface** receptor on CD4 and CD8 T cells - Recognises processed antigen in the form of linear **peptides**
59
_Generation of adaptive immune receptor by somatic recombination events_
* T and B cell receptors are produced by random recombination events between V, (D - ... chain only) and J gene segments, producing a huge receptor diversity despite a small number of genes. The most useful receptors are selected after birth upon exposure to pathogens
* T and B cell receptors are produced by random recombination events between V, (D - **heavy** chain only) and J gene segments, producing a huge receptor diversity despite a small number of genes. The most useful receptors are selected after birth upon exposure to pathogens
* We lose most of the ones we make - many don't work, some attack our own tissues etc
60
_Generation of adaptive immune receptor by somatic recombination events_
* T and B cell receptors are produced by random recombination events between ..., (... - ... chain only) and ... gene segments, producing a huge receptor diversity despite a small number of genes. The most useful receptors are selected after birth upon exposure to pathogens
* T and B cell receptors are produced by random recombination events between **V**, (**D** - **heavy** chain only) and gene segments, producing a huge receptor diversity despite a small number of genes. The most useful receptors are selected after birth upon exposure to pathogens
* We lose most of the ones we make - many don't work, some attack our own tissues etc
61
_CD8 T cells_
* ... (killer) T cells - Kill virally infected cell
* Virus infects cell - Viral proteins synthesized in cytosol - Peptide fragments of viral proteins bound by MHC class I in ER - Bound peptides transported by MHC class I to the cell surface
* On cell surface - CD8 cytotoxic lymphocyte recognises the viral peptide and kills the virally infected cell (not just any CD8 cytotoxic lymphocyte - has to have the right receptor for the viral peptide)
* **Cytotoxic** (killer) T cells - Kill virally infected cell
* Virus infects cell - Viral proteins synthesized in cytosol - Peptide fragments of viral proteins bound by MHC class I in ER - Bound peptides transported by MHC class I to the cell surface
* On cell surface - CD8 cytotoxic lymphocyte recognises the viral peptide and kills the virally infected cell (not just any CD8 cytotoxic lymphocyte - has to have the right receptor for the viral peptide)
62
_CD8 T cells_
* Cytotoxic (killer) T cells - Kill virally infected cell
* Virus infects cell - Viral proteins synthesized in cytosol - Peptide fragments of viral proteins bound by ... class I in ER - Bound peptides transported by ... class I to the cell surface
* On cell surface - CD8 cytotoxic lymphocyte recognises the viral peptide and kills the virally infected cell (not just any CD8 cytotoxic lymphocyte - has to have the right receptor for the viral peptide)
* Cytotoxic (killer) T cells - Kill virally infected cell
* Virus infects cell - Viral proteins synthesized in cytosol - Peptide fragments of viral proteins bound by **MHC** class I in ER - Bound peptides transported by **MHC** class I to the cell surface
* On cell surface - CD8 cytotoxic lymphocyte recognises the viral peptide and kills the virally infected cell (not just any CD8 cytotoxic lymphocyte - has to have the right receptor for the viral peptide)
63
_CD8 T cells_
* Cytotoxic (killer) T cells - Kill virally infected cell
* Virus infects cell - Viral proteins synthesized in cytosol - Peptide fragments of viral proteins bound by MHC class ... in ER - Bound peptides transported by MHC class ... to the cell surface
* On cell surface - CD8 cytotoxic lymphocyte recognises the viral peptide and kills the virally infected cell (not just any CD8 cytotoxic lymphocyte - has to have the right receptor for the viral peptide)
* Cytotoxic (killer) T cells - Kill virally infected cell
* Virus infects cell - Viral proteins synthesized in cytosol - Peptide fragments of viral proteins bound by **MHC class I** in ER - Bound peptides transported by **MHC class I** to the cell surface
* On cell surface - CD8 cytotoxic lymphocyte recognises the viral peptide and kills the virally infected cell (not just any CD8 cytotoxic lymphocyte - has to have the right receptor for the viral peptide)
64
_CD8 T cells_
* Cytotoxic (killer) T cells - Kill virally infected cell
* Virus infects cell - Viral proteins synthesized in cytosol - ... fragments of viral proteins bound by MHC class I in ER - Bound ... transported by MHC class I to the cell surface
* On cell surface - CD8 cytotoxic lymphocyte recognises the viral peptide and kills the virally infected cell (not just any CD8 cytotoxic lymphocyte - has to have the right receptor for the viral peptide)
* Cytotoxic (killer) T cells - Kill virally infected cell
* Virus infects cell - Viral proteins synthesized in cytosol - **Peptide** fragments of viral proteins bound by MHC class I in ER - Bound **peptides** transported by MHC class I to the cell surface
* On cell surface - CD8 cytotoxic lymphocyte recognises the viral peptide and kills the virally infected cell (not just any CD8 cytotoxic lymphocyte - has to have the right receptor for the viral peptide)
65
_CD8 T cells_
* Cytotoxic (killer) T cells - Kill virally infected cell
* Virus infects cell - Viral proteins synthesized in cytosol - Peptide fragments of viral proteins bound by ... ... ... in ER - Bound peptides transported by ... ... ... to the cell surface
* On cell surface - CD8 cytotoxic lymphocyte recognises the viral peptide and kills the virally infected cell (not just any CD8 cytotoxic lymphocyte - has to have the right receptor for the viral peptide)
* Cytotoxic (killer) T cells - Kill virally infected cell
* Virus infects cell - Viral proteins synthesized in cytosol - Peptide fragments of viral proteins bound by **MHC class I** in ER - Bound peptides transported by **MHC class I** to the cell surface
* On cell surface - CD8 cytotoxic lymphocyte recognises the viral peptide and kills the virally infected cell (not just any CD8 cytotoxic lymphocyte - has to have the right receptor for the viral peptide)
66
_CD8 T cells_
* Cytotoxic (...) T cells - ... virally infected cell
* Virus infects cell - Viral proteins synthesized in cytosol - Peptide fragments of viral proteins bound by MHC class I in ER - Bound peptides transported by MHC class I to the cell surface
* On cell surface - CD8 cytotoxic lymphocyte recognises the viral peptide and kills the virally infected cell (not just any CD8 cytotoxic lymphocyte - has to have the right receptor for the viral peptide)
* Cytotoxic (**Killer**) T cells - **kill** virally infected cell
* Virus infects cell - Viral proteins synthesized in cytosol - Peptide fragments of viral proteins bound by MHC class I in ER - Bound peptides transported by MHC class I to the cell surface
* On cell surface - CD8 cytotoxic lymphocyte recognises the viral peptide and kills the virally infected cell (not just any CD8 cytotoxic lymphocyte - has to have the right receptor for the viral peptide)
67
_CD4 T cells_
* ... T-cells
* Only respond to antigen presented by antigen-presenting cells - eg ... cell, macrophages, B-cells
* Antigen is taken up into intracellular vesicles - In early endosomes of neutral pH endosomes proteases are inactive - acidification of vesicles activates proteases to degrade antigen into peptide fragments - vesicles containing peptides fuse with vesicles containing MHC class II molecules
* Antigen presenting cell has MHC class II molecules with on surface vesicle containing peptide on groove - CD4 T cell recognises the peptide - can now tell other cells what to do
* **Helper** T-cells
* Only respond to antigen presented by antigen-presenting cells - eg **dendritic** cell, macrophages, B-cells
* Antigen is taken up into intracellular vesicles - In early endosomes of neutral pH endosomes proteases are inactive - acidification of vesicles activates proteases to degrade antigen into peptide fragments - vesicles containing peptides fuse with vesicles containing MHC class II molecules
* Antigen presenting cell has MHC class II molecules with on surface vesicle containing peptide on groove - CD4 T cell recognises the peptide - can now tell other cells what to do
68
_CD4 T cells_
* Helper T-cells
* Only respond to antigen presented by ...-...cells - eg dendritic cell, macrophages, B-cells
* Antigen is taken up into ... ... - In early endosomes of neutral pH endosomes proteases are inactive - acidification of vesicles activates proteases to degrade antigen into peptide fragments - vesicles containing peptides fuse with vesicles containing MHC class II molecules
* Antigen presenting cell has MHC class II molecules with on surface vesicle containing peptide on groove - CD4 T cell recognises the peptide - can now tell other cells what to do
* Helper T-cells
* Only respond to antigen presented by **antigen-presenting** cells - eg dendritic cell, macrophages, B-cells
* Antigen is taken up into **intracellular vesicles** - In early endosomes of neutral pH endosomes proteases are inactive - acidification of vesicles activates proteases to degrade antigen into peptide fragments - vesicles containing peptides fuse with vesicles containing MHC class II molecules
* Antigen presenting cell has MHC class II molecules with on surface vesicle containing peptide on groove - CD4 T cell recognises the peptide - can now tell other cells what to do
69
_CD4 T cells_
* Helper T-cells
* Only respond to antigen presented by antigen-presenting cells - eg dendritic cell, macrophages, B-cells
* Antigen is taken up into intracellular vesicles - In early endosomes of neutral pH endosomes proteases are inactive - acidification of vesicles activates proteases to degrade antigen into ... fragments - vesicles containing ... fuse with vesicles containing MHC class ... molecules
* Antigen presenting cell has MHC class ... molecules with on surface vesicle containing peptide on groove - CD4 T cell recognises the peptide - can now tell other cells what to do
* Helper T-cells
* Only respond to antigen presented by antigen-presenting cells - eg dendritic cell, macrophages, B-cells
* Antigen is taken up into intracellular vesicles - In early endosomes of neutral pH endosomes proteases are inactive - acidification of vesicles activates proteases to degrade antigen into **peptide** fragments - vesicles containing peptides fuse with vesicles containing MHC class **II** molecules
* Antigen presenting cell has MHC class **II** molecules with on surface vesicle containing peptide on groove - CD4 T cell recognises the peptide - can now tell other cells what to do
70
_CD4 T cells_
* Helper T-cells
* Only respond to antigen presented by antigen-presenting cells - eg dendritic cell, macrophages, B-cells
* Antigen is taken up into intracellular vesicles - In early endosomes of neutral pH endosomes proteases are inactive - acidification of vesicles activates proteases to degrade antigen into peptide fragments - vesicles containing peptides fuse with vesicles containing ... ... ... molecules
* Antigen presenting cell has ... ... ... molecules with on surface vesicle containing peptide on groove - CD4 T cell recognises the peptide - can now tell other cells what to do
* Helper T-cells
* Only respond to antigen presented by antigen-presenting cells - eg dendritic cell, macrophages, B-cells
* Antigen is taken up into intracellular vesicles - In early endosomes of neutral pH endosomes proteases are inactive - acidification of vesicles activates proteases to degrade antigen into peptide fragments - vesicles containing peptides fuse with vesicles containing **MHC class II molecules**
* Antigen presenting cell has **MHC class II** molecules with on surface vesicle containing peptide on groove - CD4 T cell recognises the peptide - can now tell other cells what to do
71
_CD4 T cells_
* Helper T-cells
* Only respond to antigen presented by antigen-presenting cells - eg dendritic cell, macrophages, B-cells
* Antigen is taken up into intracellular ... - In early endosomes of neutral pH endosomes proteases are inactive - acidification of ... activates proteases to degrade antigen into peptide fragments - ... containing peptides fuse with ... containing MHC class II molecules
* Antigen presenting cell has MHC class II molecules with on surface ... containing peptide on groove - CD4 T cell recognises the peptide - can now tell other cells what to do
* Helper T-cells
* Only respond to antigen presented by antigen-presenting cells - eg dendritic cell, macrophages, B-cells
* Antigen is taken up into intracellular **vesicles** - In early endosomes of neutral pH endosomes proteases are inactive - acidification of **vesicles** activates proteases to degrade antigen into peptide fragments - **vesicles** containing peptides fuse with **vesicles** containing MHC class II molecules
* Antigen presenting cell has MHC class II molecules with on surface **vesicle** containing peptide on groove - CD4 T cell recognises the peptide - can now tell other cells what to do
72
_Clonal selection_
* What is it?
Clonal selection is a process proposed to explain how a single B or T cell that recognizes an antigen that enters the body is selected from the pre-existing cell pool of differing antigen specificities and then reproduced to generate a clonal cell population that eliminates the antigen.
73
_T and B cell memory_
* After primary infection, most clonally-expanded T and B lymphocytes die off; a few remain as long-lived ... cells
*
* After primary infection, most clonally-expanded T and B lymphocytes die off; a few remain as long-lived **memory cells**
* Antigen A injected - measure antibody against antigen a or count no of T cells specific for A - nothing happens for a few days, then response to Antigen A, plateau then not back to baseline - meet antigen A again - remains at high level - faster, steeper antibody response - shows Primary vs Secondary immune responsecells
74
_T and B cell memory_
* After primary infection, most clonally-expanded T and B lymphocytes die off; a few remain as long-lived ... cells
*
* After primary infection, most clonally-expanded T and B lymphocytes die off; a few remain as long-lived **memory cells**
* Antigen A injected - measure antibody against antigen a or count no of T cells specific for A - nothing happens for a few days, then response to Antigen A, plateau then not back to baseline - meet antigen A again - remains at high level - faster, steeper antibody response - shows Primary vs Secondary immune responsecells
75
_Effector mechanisms: some examples_
* ... (skin, acid pH in gut etc etc)
* Cytokines
* Complement
* Phagocytosis (enhanced by opsonisation)
* Cytotoxicity (CD8 T cell, NK cell)
* Antibody-dependent cellular cytotoxicity
* Mast cell and eosinophil degranulation
* *Effector mechanisms are shared between innate and adaptive immunity - adaptive immunity is defined by it's receptors not by it's effector mechanisms*
* **Barriers** (skin, acid pH in gut etc etc)
* Cytokines
* Complement
* Phagocytosis (enhanced by opsonisation)
* Cytotoxicity (CD8 T cell, NK cell)
* Antibody-dependent cellular cytotoxicity
* Mast cell and eosinophil degranulation
* *Effector mechanisms are shared between innate and adaptive immunity - adaptive immunity is defined by it's receptors not by it's effector mechanisms*
76
_Effector mechanisms: some examples_
* Barriers (..., ... pH in gut etc etc)
* Cytokines
* Complement
* Phagocytosis (enhanced by opsonisation)
* Cytotoxicity (CD8 T cell, NK cell)
* Antibody-dependent cellular cytotoxicity
* Mast cell and eosinophil degranulation
* *Effector mechanisms are shared between innate and adaptive immunity - adaptive immunity is defined by it's receptors not by it's effector mechanisms*
* Barriers (**skin, acid** pH in gut etc etc)
* Cytokines
* Complement
* Phagocytosis (enhanced by opsonisation)
* Cytotoxicity (CD8 T cell, NK cell)
* Antibody-dependent cellular cytotoxicity
* Mast cell and eosinophil degranulation
* *Effector mechanisms are shared between innate and adaptive immunity - adaptive immunity is defined by it's receptors not by it's effector mechanisms*
77
_Effector mechanisms: some examples_
* Barriers (skin, acid pH in gut etc etc)
* Cytokines
* Complement
* ... (enhanced by opsonisation)
* ... (CD8 T cell, NK cell)
* Antibody-dependent cellular cytotoxicity
* Mast cell and eosinophil degranulation
* *Effector mechanisms are shared between innate and adaptive immunity - adaptive immunity is defined by it's receptors not by it's effector mechanisms*
* Barriers (skin, acid pH in gut etc etc)
* Cytokines
* Complement
* **Phagocytosis** (enhanced by opsonisation)
* **Cytotoxicity** (CD8 T cell, NK cell)
* Antibody-dependent cellular cytotoxicity
* Mast cell and eosinophil degranulation
* *Effector mechanisms are shared between innate and adaptive immunity - adaptive immunity is defined by it's receptors not by it's effector mechanisms*
78
_Effector mechanisms: some examples_
* Barriers (skin, acid pH in gut etc etc)
* C...
* C...
* Phagocytosis (enhanced by opsonisation)
* Cytotoxicity (CD8 T cell, NK cell)
* Antibody-dependent cellular cytotoxicity
* Mast cell and eosinophil degranulation
* *Effector mechanisms are shared between innate and adaptive immunity - adaptive immunity is defined by it's receptors not by it's effector mechanisms*
* Barriers (skin, acid pH in gut etc etc)
* **Cytokines**
* **Complement**
* Phagocytosis (enhanced by opsonisation)
* Cytotoxicity (CD8 T cell, NK cell)
* Antibody-dependent cellular cytotoxicity
* Mast cell and eosinophil degranulation
* *Effector mechanisms are shared between innate and adaptive immunity - adaptive immunity is defined by it's receptors not by it's effector mechanisms*
79
_Effector mechanisms: some examples_
* Barriers (skin, acid pH in gut etc etc)
* Cytokines
* Complement
* Phagocytosis (enhanced by opsonisation)
* Cytotoxicity (CD8 T cell, NK cell)
* Antibody-dependent cellular cytotoxicity
* ... cell and ... degranulation
* *Effector mechanisms are shared between innate and adaptive immunity - adaptive immunity is defined by it's receptors not by it's effector mechanisms*
* Barriers (skin, acid pH in gut etc etc)
* Cytokines
* Complement
* Phagocytosis (enhanced by opsonisation)
* Cytotoxicity (CD8 T cell, NK cell)
* Antibody-dependent cellular cytotoxicity
* **Mast** cell and **eosinophil** degranulation
* *Effector mechanisms are shared between innate and adaptive immunity - adaptive immunity is defined by it's receptors not by it's effector mechanisms*
80
_Effector mechanisms: some examples_
* Barriers (skin, acid pH in gut etc etc)
* Cytokines
* C...t
* Phagocytosis (enhanced by ...)
* Cytotoxicity (CD8 T cell, NK cell)
* Antibody-dependent cellular cytotoxicity
* Mast cell and eosinophil degranulation
* *Effector mechanisms are shared between innate and adaptive immunity - adaptive immunity is defined by it's receptors not by it's effector mechanisms*
* Barriers (skin, acid pH in gut etc etc)
* Cytokines
* **Complement**
* Phagocytosis (enhanced by **opsonisation**)
* Cytotoxicity (CD8 T cell, NK cell)
* Antibody-dependent cellular cytotoxicity
* Mast cell and eosinophil degranulation
* *Effector mechanisms are shared between innate and adaptive immunity - adaptive immunity is defined by it's receptors not by it's effector mechanisms*
81
_Acute Inflammation_
* Inflamito – setting alight
* Cardinal features: ..., ..., red, swollen
* Describes a process, but tells you nothing of the cause
* Blood vessel changes underlie the process
* Vasodilatation
* Adhesion molecules
* Increased permeability
* The clinical features are therefore defined by an interaction between the pathogen and host immunity
* Inflamito – setting alight
* Cardinal features: **hot, painful,** red, swollen
* Describes a process, but tells you nothing of the cause
* Blood vessel changes underlie the process
* Vasodilatation
* Adhesion molecules
* Increased permeability
* The clinical features are therefore defined by an interaction between the pathogen and host immunity
82
_Acute Inflammation_
* Inflamito – setting alight
* Cardinal features: hot, painful, red, swollen
* Describes a ..., but tells you nothing of the ...
* ... ... changes underlie the process
* Vasodilatation
* Adhesion molecules
* Increased permeability
* The clinical features are therefore defined by an interaction between the pathogen and host immunity
* Inflamito – setting alight
* Cardinal features: hot, painful, red, swollen
* Describes a **process**, but tells you nothing of the **cause**
* **Blood vessel** changes underlie the process
* Vasodilatation
* Adhesion molecules
* Increased permeability
* The clinical features are therefore defined by an interaction between the pathogen and host immunity
83
_Acute Inflammation_
* Inflamito – setting alight
* Cardinal features: hot, painful, red, swollen
* Describes a process, but tells you nothing of the cause
* Blood vessel changes underlie the process
* V...
* ... molecules
* Increased permeability
* The clinical features are therefore defined by an interaction between the pathogen and host immunity
* Inflamito – setting alight
* Cardinal features: hot, painful, red, swollen
* Describes a process, but tells you nothing of the cause
* Blood vessel changes underlie the process
* **Vasodilatation**
* **Adhesion** molecules
* Increased permeability
* The clinical features are therefore defined by an interaction between the pathogen and host immunity
84
_Acute Inflammation_
* Inflamito – setting alight
* Cardinal features: hot, painful, red, ...
* Describes a process, but tells you nothing of the cause
* Blood vessel changes underlie the process
* Vasodilatation
* ... molecules
* Increased ...
* The clinical features are therefore defined by an interaction between the pathogen and host immunity
* Inflamito – setting alight
* Cardinal features: hot, painful, red, **swollen**
* Describes a process, but tells you nothing of the cause
* Blood vessel changes underlie the process
* Vasodilatation
* **Adhesion** molecules
* Increased **permeability**
* The clinical features are therefore defined by an interaction between the pathogen and host immunity
