Lecture 5- Immune mechanisms: adaptive immunity Flashcards
examples of adaptive receptors which antigens can respond to
antibodies, B cell and T cell receptors
lymphocyte division rates
about once every 12 hours (can be maintained for weeks), once per 6h at the absolute most
differences between primary and secondary infection wrt adaptive response
primary- much slower for adaptive processes to kick in (week/2)
secondary- quicker, takes 2-4 days for a peak response
what is an antibody
soluble form of the B cell receptor
how are TCRs formed
rearrangement of genomic segments, e.g. through recombination
term for the large amount of receptors generated
anticipatory repertoire
how does receptor selection occur
clonal distribution of receptors, testing for inappropriate activation, killing off of these ‘inappropriate’ cells
how do T cells develop
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
how can B cell class switches occur
changes in antibody production at the constant region of Ig- e.g. IgE into IgA
difference in what MHCs lead to what T cell being produced
CD4+- MHC II
CD8+- MHC I
gammadelta T cells
can do either the cytotoxic or helper functions
subdivisions of CD8+ cells
Tc1 and 2, depending on cytokine production
subdivision of CD4+ cells
based on cytokine production mostly- e.g. Th17 producing IL-17
Treg cell cytokine production
IL-10, inhibits some cytokines so prevents Th activation (12/23)
names of different activation pathways
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
3 types of professional APC
dendritic cells, macrophages, B cells
CD8 cell terminal phenotype
IFNγ producing cytotoxic capable cells, containing enzymes such as granzymes A and B and perforin
differences between individual CD8 cells
different ‘levels’ of the terminal phenotype, e.g. may be ‘single’ - ‘total’ producers
3 cytotoxic molecules
granzyme A/B (activate cytotoxic pathways)
perforin (hole)
granylysin (activates apoptosis, direct antibiotic effects)
CD4 vs 8 memory
CD8 memory seems more stable
-however may not be universal, found higher selective deletion of CD8 memory cells in a mouse infection (Varga 2001)
2 types of CD8 memory pool
effector memory (fast effectors, depleted quicker)
central memory (stick around, but need to proliferate before they can do much)
Th1 cells
IL-2 and TFNbeta
activate macrophages
Treg cells
IL-20 and TGFbeta
down-regulate other T cell responses
how can Th subsets be differentiated
naive cells stimulated with signalling molecules such as IL-12
