B Cells & Antibodies Flashcards
(32 cards)
The diversity of both chains of the BCR/antibody comes from…
rearranging gene segments on chromosome 14 (one from mom, one from dad)
Four different gene segments for BCRs
V, D, J, and C
T or F. Both chromosome 14 works to make a BCR
F! only the chromosome that gets a working combination gets the job! other chromosome shuts down
T or F. The Hc is produced first
T!
- process is repeated for Lc and Hc and Lc have to fit together as final test
Two interacting components of how a BCR signals
- pathogen is recognized by epitope (50-79 AAs long) binding to the Hc and Lc ‘antennae’
- proteins IgA and IgB transmit a signal to let the B cell know to turn on its Ab-making
The concept of cross-linking (how the BCR signals)
- polymeric antigen: repeats of an epitope can bind multiple BCRs and bring them together, also many copies of the same antigen can do this
- complement receptors on the B cell recognize a fragment of iC3b, enhancing the clustering that occurs with BCRs - amplifies B cell signalling by 100-fold; acts as a co-receptor
Second signals for B cell activation
with or without Th help!
What is the first signal in B cell activation?
cross-linking or clustering
The second or co-stimulatory signal for B cell activation is crucial as it determines the _______ of the B cell response.
quality
T cell-dependent activation second signal
CD40 on the B cell binds to CD40L on Th cell AKA CD154
T cell-independent activation second signal
involves interaction with a ‘danger signal’, most likely by recognition of PAMPs by Toll-like receptors or other PRRs
Advantages of T-independent B cell response
- fast; don’t need for Th cells to be activated themselves
2. can respond to non-protein antigens
Why does the T-independent B cell response need two signals for activation?
the second co-stimulatory signal helps prevent B cells from being activated against polymers from our own bodies like our DNA
Third way to stimulate B cells
- mitogens
- can bind to molecules on B cells that happen to be associated with BCRs = clustering!
- clustering occurs independent of any antigen recognition by the BCR = activation of many B cells = polyclonal = many clones of B cells are activated this way
- not what we want! some parasites use this to confuse our immune system
Maturation of B cells
- class switching
- somatic hypermutation
- career decision
when genes for the BCR undergo mutations that increase the affinity of the BCR for its cognate antigen
somatic hypermutation
cutting and pasting Hc genes on chromosome 14 leads to changes in …
antibody class
Like five IgG structures held together by a J chain
IgM
This antibody is very good at activating the complement classical pathway
IgM
- does this by allowing two C1qrs protein complexes to come together via its Fc region when IgM binds to its cognate antigen on an invader
- the C1s lose their inhibitor molecule which leads to activation of a C3 convertase
This antibody class is a good neutralizer and can cross the placenta and protect a fetus
IgG
Half life of IgM vs IgG
one day vs three weeks
The most abundant class of antibody in the blood
IgG
Subclasses of IgG
- IgG3 fixes complement well, and can be recognized by NK cells (ADCC
- IgG1 is a great opsonizer and cna enhance phagocytosis
Most abundant antibody of all
IgA
- rare in blood but very common on mucosal surfaces and in mucosal secretions
