Lecture 5- Immune mechanisms: adaptive immunity Flashcards

1
Q

examples of adaptive receptors which antigens can respond to

A

antibodies, B cell and T cell receptors

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2
Q

lymphocyte division rates

A

about once every 12 hours (can be maintained for weeks), once per 6h at the absolute most

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3
Q

differences between primary and secondary infection wrt adaptive response

A

primary- much slower for adaptive processes to kick in (week/2)
secondary- quicker, takes 2-4 days for a peak response

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4
Q

what is an antibody

A

soluble form of the B cell receptor

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5
Q

how are TCRs formed

A

rearrangement of genomic segments, e.g. through recombination

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6
Q

term for the large amount of receptors generated

A

anticipatory repertoire

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7
Q

how does receptor selection occur

A

clonal distribution of receptors, testing for inappropriate activation, killing off of these ‘inappropriate’ cells

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8
Q

how do T cells develop

A

thymic selection- need to recognise the MHC, cell death by neglect where this recognition does not occur
filtering for autoreactive cells
testing response to the pathogen- passing activation threshold > can divide

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9
Q

how can B cell class switches occur

A

changes in antibody production at the constant region of Ig- e.g. IgE into IgA

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10
Q

difference in what MHCs lead to what T cell being produced

A

CD4+- MHC II
CD8+- MHC I

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11
Q

gammadelta T cells

A

can do either the cytotoxic or helper functions

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12
Q

subdivisions of CD8+ cells

A

Tc1 and 2, depending on cytokine production

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13
Q

subdivision of CD4+ cells

A

based on cytokine production mostly- e.g. Th17 producing IL-17

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14
Q

Treg cell cytokine production

A

IL-10, inhibits some cytokines so prevents Th activation (12/23)

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15
Q

names of different activation pathways

A

endogenous- MHC I and CD8- involves sampling cytoplasm (but dendritic cells can present extracellular antigens through this process, as they need to)
exogenous- MHC II and CD4- involves sampling extracellular compartment, mostly of APCs

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16
Q

3 types of professional APC

A

dendritic cells, macrophages, B cells

17
Q

CD8 cell terminal phenotype

A

IFNγ producing cytotoxic capable cells, containing enzymes such as granzymes A and B and perforin

18
Q

differences between individual CD8 cells

A

different ‘levels’ of the terminal phenotype, e.g. may be ‘single’ - ‘total’ producers

19
Q

3 cytotoxic molecules

A

granzyme A/B (activate cytotoxic pathways)
perforin (hole)
granylysin (activates apoptosis, direct antibiotic effects)

20
Q

CD4 vs 8 memory

A

CD8 memory seems more stable
-however may not be universal, found higher selective deletion of CD8 memory cells in a mouse infection (Varga 2001)

21
Q

2 types of CD8 memory pool

A

effector memory (fast effectors, depleted quicker)
central memory (stick around, but need to proliferate before they can do much)

22
Q

Th1 cells

A

IL-2 and TFNbeta
activate macrophages

23
Q

Treg cells

A

IL-20 and TGFbeta
down-regulate other T cell responses

24
Q

how can Th subsets be differentiated

A

naive cells stimulated with signalling molecules such as IL-12

25
Q

important fact about Th cell differentiation

A

can be plasticity- reprogramming etc is common

26
Q

another type of TCRαβ cell

A

invariant natural killer T cells
act as an early source of cytokines like NK cells, but different pathway of activation and no evidence of memory

27
Q

TCRγδ cells- function

A

recognise different things compared to ab cells
earliest T cells in the thymus- important in early life?