B lymphocyte

B cells (named after the bursa of Fabricius, where they were discovered in birds) develop in the bone marrow. Pro-B cells rearrange their heavy-chain genes (D–J, then V–DJ) using RAG1/RAG2, with TdT adding junctional diversity; pre-B cells express the heavy chain with a surrogate light chain (the pre-BCR), whose signalling through Bruton tyrosine kinase (BTK) permits proliferation and light-chain (κ, then λ) rearrangement. Immature B cells express surface IgM; those binding self-antigen strongly undergo receptor editing, deletion or anergy (central tolerance). Survivors migrate to the spleen and mature into naive follicular B cells co-expressing IgM and IgD.

The B-cell receptor (BCR) is membrane immunoglobulin associated with the signalling chains Igα/Igβ (CD79a/CD79b), with a co-receptor complex (CD19, CD21 — the complement receptor CR2, also used by EBV — and CD81). B-cell markers include CD19, CD20 (target of rituximab) and CD22. Unlike T cells, B cells recognise native, unprocessed antigen of any chemical type (proteins, polysaccharides, lipids, nucleic acids).

T-independent antigens (e.g. bacterial capsular polysaccharides with repeating epitopes) cross-link many BCRs and activate B cells — particularly marginal-zone and B-1 cells — without T-cell help, producing mainly IgM, little class switching and weak memory; infants under about 2 years respond poorly to them. T-dependent (protein) antigens are internalised by the BCR, processed and presented on MHC class II to a helper T cell recognising the same antigen; the T cell provides CD40L–CD40 contact and cytokines (IL-4, IL-21). The B cell then forms early extrafollicular plasmablasts or enters a germinal centre, where somatic hypermutation, affinity maturation and class switching occur (IFN-γ favours IgG subclasses, IL-4 favours IgE, TGF-β favours IgA), producing long-lived plasma cells and memory B cells.