L2 Immune recognition Flashcards
what are the two types of recognition molecules
B cells (B cell receptor/immunoglobulin) T cells (TCR)
what is the B cell immunoglobulin structure
2 heavy 2 light chains, constant and variable domains at the two combining site - antigen binding
Hinge
how come B cell immunoglobulins move to bind to target
have a hinge
what is the T cell receptor structure
Alpha and beta chain has constant (close to cell surface) and variable domain – only one antigen combining site made of variable alpha and beta chain
what is the difference between B and T cell recognition
T cell cant directly recognise need info presented to them via antigen presenting cell
how do B cells recognise
surface Ig – bind directly to pathogen /antigen
what happens to B cell following recognition
B cell activated makes plasma cells = lots more Ig which all bind to the pathogen
how do T cells recognise
needs info of pathogen processed and presented to it via MHC
antigen presenting cells do this e.g. dendritic cells
what happens to T cell following recognition
effector cell activated – might be CD4 or CD8 (depends on the MHC)
where is there variability the variable domains
areas of hypervariability – variation between amino acid structure is huge = will recognise a different target
3 areas of hypervariability in heavy and light
how are B cells activated
only through B cell clustering
Ig alpha and Ig beta have capacity to signal to cell to become activated – have tyrosine receptor molecules to intracellulary activate Ig alpha and beta molecules found in conjunction with B cell receptor
why cant the B cell become activated by itself
might be a chance encounter with antigen or might bind to a target not specifically – can’t have this or adaptive response and B cells constantly activated
what does BCR complex clustering cause
lots of B cells bind to target = B cell receptor clustering
turns on Ig alpha and beta signal B cell to start making lots of antibodies
what is the BCR co-receptor complex
second signal through complement receptors binding to complement that has opsonized the pathogen
what is needed for B cell to make antibodies
BCR clustering and BCR co-receptor complex
what is the TCR for
not able to signal only there for indirect recognition via antigen presenting cell
what are the two classes of TCR
alpha beta
gamma delta
what are the T cell co-receptors
CD$
CD8
what is the structure of the CD4 receptor
one chain
what is the structure of the CD8 receptor
one alpha one beta molecule in separate chains
what does the helper T cell express
helper T cell expresses CD4 alongside T cell receptor
what does the cytotoxic T cell express
cytotoxic T cell expresses CD8 alongside T cell receptor
what does MHC class I present to
CD8
what does MHC class II present to
CD4
when does the T cell kill the pathogen
virus gone into the cell on its own *infected will be in cytosol
virally infected cell
T cell by MHC I – bind to CD8 co receptor T cell – to kill it
when is the T helper cell activated
pathogen deliberately taken into cell via phagocytosis will be in vesicle
T cell with CD4 co receptor will bind = helper T cell activated to help clear it
what can MHCI present
small peptides 8-10 amino acids to CD8 cell
what can MHCII present
larger at least 13 amino acid epitope to CD4
what is the CD3 complex function
has activation motifs inside cell that activate T cell to carry out its effector function
what is the CD3 co-receptor function
CD3 and co-receptor complex comes together to signal and activate the T cell
where are cytosolic pathogens degraded
cytosol
what peptides bind to a cytosolic pathogen
MHCI
what T cell are cytosolic pathogens presented to
CD8
what happens to cytosolic pathogens
killed - cell death
where are intravesicular pathogens degraded in
endocytic vesicles
what peptides bind to intravesicular pathogens
MHCII
what T cell are intravesicular pathogens presented to
CD4
what happens to intravesicular pathogens
activation to kill intravesicular bacteria and parasites
where are extracellular pathogens and toxins degraded
endocytic vesicles
which peptides bind to extracellular pathogens and toxins
MHCII
what are extracellular pathogens and toxins presented to
CD4
what happens to extracellular pathogens and toxins
activation of B cells to secrete Ig - eliminate them
why do other non innate cells have MHCI
any cell could be infected by virus so not just innate cells with MHC I
what happens in MHCI processing and presentation
proteasome degrades antigen in cytosol – pieces taken to endoplasmic reticulum
MHCI load info onto cell surface = activate CD8 cytotoxic T cell
phagocytosis - degraded in vesicle
where is MHCII made
made in endoplasmic reticulum
what happens to MHCII invariant chain
has an invariant chain bound to it, when leaves endoplasmic reticulum is cleaved in vesicle
what is important in blood transfusion
need to have HLA matching in transplantation
