Rapid response, but no isotype switching or somatic hypermutation.
No memory cells.
T-dependent B cells
Cross linking of BCR can initiate activation, but cannot induce differentiation and antibody production unless also receives T cell help.
CD40( R) on B cell receives signal from CD40L on effector Th.
T cell help induces class switching, somatic hypermutation, differentation into plasma, memory cells.
Properties of Td antigens
Must be able to get T cell help, so must have peptides.
Must be perceived as “non-self”. Why?
Must be large and complex enough to be able to cross-link BCR, and to contain both B and T cell epitopes.
Route of entry
Ingested tends to produce active IgA response in mucosa, but inhibits IgG production in lymph.
Three signal model of B cell activation Signal 1: Conveyed into cytopolasm by Ig alpha, beta Upregulates MHC II, CD40, cytokine receptors. If second signal not received, apoptoses or becomes “anergic”.
Linked Recognition Signal 2: T cell epitope must be linked to B cell epitope! So can you activate a B cell against, say, DNA? How? Signal 3: Th cell reorients cytoplasm; releases cytokines only on side of cell making contact. Division; differentiation into plasma cells or memory cells.
Lymph node follicles
Most interaction between B cells, antigen and Th occurs in “follicles” in lymph nodes and spleen.
Follicular Dendritic Cells coated with antigen
Switch between membrane bound vs secreted via RNA Processing/Differential Splicing
Class [isotype] switching: After antigen stimulation w T cell help Hyper-IgM syndromes: No isotype switching or somatic hypermutation.
If dividing follicular B cell receives sustained Bcl-6 signaling, becomes a memory cell.
If Bcl-6 drops off, plasma cell.
Expanded rER, Golgi
Little or no CD40, MHC II, BCR
Migrate to lymph nodes, spleen, bone marrow, and continue secreting antibodies, for several months.
Up to 40% of total protein synthesis is antibodies.
NK, eosinophils cytotoxic.
Ch 5 Self-test questions you should be able to answer: