lecture 6 - B cell activation Flashcards
activated can become what two cells
plasma or memory cells
plasma cells release their
BCR
roles of antibodies:
1. neutralisation
antibodies bind to the pathogen preventing it from affecting our cells
- opsonization
antibodies bind to pathogen and promotes phagocytes to engulf it
- activates the complement system
enhances opsonization and puts hole in pathogens
naive B cells express which BCRs
IgM or IgD
BCR binding to an antigen provides
signal 1 to a B cell
Igα and Igβ have what motifs in its cytoplasmic regions
ITAM (immunoreceptor tyrosine-based activation motif)
CD3 also has ITAMS. ITAMs have what residues
tyrosine
it is likely that the antigen is coated in what
complement
the complement can interact with what
Complement recepto3 3 on b cell surface
if this happens theres a bigger signal, why?
becuase you get a signal from the BCR and the CR2
thymus-independent antigens:
signal 2 is provided by
the antigen itself or extensive cross linking
thymus dependent antigen:
signal 2 is provided by
CD4 t cells
thymus independent antigens lead to which antibody production
only IgM (never class switches)
TI-1 antigens provide the second signal by
binding to other receptors on the b cells
TI-2 antigens contain repeated epitopes and they will do what
cross-link many BCR on the same B cell surface
this massively amplifies signal 1 (doesnt give a signal 2)
thymus dependent antigens:
BCR binds antigen (signal 1) and it then internalises the antigen and presents it on MHC class II to the CD4 T cells and receives signal 2 by
CD40/CD40-L interaction
why can all classes antibodies be produced from an TD antigen
because cytokines secreted by T cell help b cell to class switch
CD40-L is on the
T cell
CD40 is on the
B cell
epitopes recognised by the antibody and the T cell are different but they are
physically linked
how to convert a TI antigen to a TD antigen:
add a protein to the polysaccharide, the antigen will be internalised and peptides presented will include
the peptide added and the antigen
this called a conjugate vaccine
inside B cell follicles, B cells are rapidly proliferating in the
germinal centres (GC)
B cells divide rapidly to become
centroblasts
centroblasts undergo
somatic hypermutation (due to AID increasing or decreasing its affinity) causing isotype switching
they then stop dividing and get smaller and these are called
centrocytes
once the B cell has its second signal from the t cell it enters the
b cell follicle
the dark zone is where?
the B cells are rapidly proliferating
some centrocytes move out of dark zone to the
light zone
follicular dendritic cells are in the light zone and the have antigen on their surface.
some t cells become T fh cells and they will follow the b cell into the light zone
the centrocytes will take up the antigen from the FDC if its affinity has improved after somatic hypermutation and present it to the T fh cell and the Tfh selects the B cells with the best BCR and the Tfh helps the b cells become memory and plasma cells
ones with decreased affinity to the antigen undergo apoptosis or go back into the dark zone and try again
what region does the somatic mutation
V region
T fh cells help the B cells can secrete Th1 and Th2 type
cytokines
CD40 signal induces what
isotype switching
AID also tells the b cell to start breaking its DNA to put the hyper mutated VDJ with
a different constant region so the b cell changes from IgM/D to IgG,A or E
cytokines from T fh cell tells b cell which isotype to become
