TLRs, MHC and activation of T cells

there are multiple types of receptors. how are these specific?

bind/recognise specific features of microbes/pathogens to trigger phagocytosis

what is the FcR? (stands for what)

Fc receptor

what is the CR? (stands for what)

complement receptor

what is the MR? (stands for what)

mannose receptor

what does the Fc receptor do

binds to the Fc region of antibody

what allows binding in an Fc receptor?

conformational change

what does the complement receptor recognise?

C3B complement bound to surface of antigen

what are the two receptor types that recognise microbes when tagged with antibody or complement attached to antigen?

Fc receptor, complement receptor

what receptor recognises microbes based on intrinsic structures?

mannose receptor

what does the mannose receptor recognise?

highly branched mannose structures on microbes (bacteria and yeast)

what is opsonisation?

opsonins are added as tags to pathogens and dead cells to make them more recognisable for phagocytosis

what are PAMPs?

pathogen associated molecular patterns

what are DAMPs?

damage associated molecular patterns

what do pattern recognition receptors recognise?

PAMPs and DAMPs

what are the 3 recognition mechanisms of toll like receptors (TLRs)

methylation, bacterial membranes, flagellum of motile bacteria

how do TLRs use methylation to recognise pathogens?

bacterial DNA is undermethylated compared to host DNA

how do TLRs use bacterial membranes to recognise pathogens?

lipopolysaccharide in gram-negative bacteria, lipoteichoic acid (LTA) in gram-positive bacteria

where are TLRs present?

plasma membrane and endosomes

what happens as a result of TLR dimerisation?

adaptor proteins are recruited and these activate signal cascades that alter transcription of inflammatory genes

what does MHC stand for

major histocompatibility complex

what cells express MHC1?

all nucleated cells

what cells express MHC2?

antigen presenting cells

what binds to MHC1?

peptides generated in the cytoplasm (endogenous source)

what binds to MHC2?

peptides generated in acidic vesicles (exogenous source)

where do polymorphisms occur in MHC?

only in the peptide binding sites (binding cleft)

why is self peptide/antigen required?

MHC is only stable when bound to antigen so when there’s no infection it needs something to bind to

what is signal 1 for the activation of T cells?

presentation of peptide on MHC on the dendritic cell and the recognition of this by the T cell

what is signal 2 for the activation of T cells?

interaction between CD80 on the dendritic cell and CD28 on the T cell

what signal(s) are present for a naïve T cell to induce the Anergy/apoptosis response?

only signal 1, not signal 2

what signal(s) are present for a naïve T cell to induce the activated state and response?

both signal 1 and 2

what happens to the T cell if anergy state is induced?

no proliferation of the T cell and no production of interleukin 2

what happens to the T cell if activation state is induced?

T cell proliferates and there is production of interleukin 2