CoachA naive T cell is activated when its receptor binds peptide–MHC on a dendritic cell that also provides costimulation (Chapter 15); it then divides every six to eight hours for a week and differentiates. CD4 helper T cells differentiate, according to the dendritic cell’s cytokines, into subsets: Th1, which activate macrophages to kill what they have eaten (tuberculosis); Th2, which drive IgE and eosinophils against worms; Th17, which recruit neutrophils against extracellular bacteria and fungi; follicular helpers, which help B cells; and regulatory T cells, which suppress. CD8 cytotoxic T cells kill cells displaying their peptide on class I, by perforin and granzymes and by the Fas ligand, triggering apoptosis (Chapter 10) — the defence against viruses and tumours. A B cell is activated by antigen binding its receptor plus help from a follicular helper T cell that recognises peptides of the same antigen on the B cell’s class II; it then becomes a plasma cell secreting thousands of antibodies a second, for days (short-lived, in the node) or years (long-lived, in the marrow), or enters a germinal centre. Memory B and T cells — long-lived, more numerous than the naive precursors and quicker to respond — are the residue of every response and the basis of vaccination.
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Example 16.7 (Kinetics of a response)
About one B cell in binds a given epitope, so a body’s B cells hold some precursors, of which perhaps a hundred meet the antigen in the draining node. Dividing every eight hours, a hundred cells become in a week. Antibody appears in the serum after four to six days, IgM first, peaks at about two weeks and declines with a half-life of three weeks for IgG as the short-lived plasma cells die, settling at the level the long-lived marrow plasma cells maintain for years. A second exposure starts from – memory cells of high affinity already switched to IgG: antibody rises within two days, ten- to a hundredfold higher, and neutralises the pathogen before it can establish itself — which is what a vaccine buys.