see also B cell maturation and B cell activation

B cells recognize native, non-processed antigen and generate antibodies in response to them in contrast to T cells which recognize processed antigen. B cells are antigen-presenting cells. The B cell receptor (BCR) cross-linking induces antigen internalization to endosomes. Antigen is then proteolysed to peptides which associate with MHC class II. MHC class II-peptide complexes traffic to surface of the B cell. B cells present antigen recognized by thier BCR 105 times more efficiently than other antigens.

Types of B cells:

Plasma Cells: are antibody secreting B cells.

Memory B cells: These B cells have secondary Ab resposnes which are faster and of greater magnitude than primary responses. This may be due to 1) increased T cell help, 2) numbers of antigen specific B cells due to clonal expansion, 3) increased affinity of antigen specific B cells due to affinity maturation in germinal centers and 4) intrinsic differences in memory B cells that allow more rapid differentiation to plasma cells due to differences in cytoplasmic domains of IgG vs IgM/D and upregulation of TLRs.

B1B cells: a separate lineage of B cells found mianly in the peritoneal cavity. They make rapid response to bacterial antigens. B1B cells are key for bacterial response. They have different cytokine requirements. B1B cells are insensitive to the absence of FL and less sensitive to the absence of IL7R. However, they are absent in triple deficient mice.

Effect of B cell on nonspecific cell mediated responses:

In some cases, antibodies produced during the humoral response can influence cell mediated responses. For example, both macrophages and NK cells have membrane receptors than can bind the carboxyl terminal end of an antibody molecule which allows these cells to interact with the foreign cell in a process known as antibody dependent cell mediated cytotoxicity (ADCC). The antibody provides the specificity but killing is mediated by the nonspecific macrophage or NK cell. Different types of constant regions may bind different Fc receptors. Examples include the binding of IgG1 Fc domains to cognate Fc receptors CD16 (FcyRIII), CD32 (FcalphaRII-B1 and -B2), and CD64 (FcalphaRI), IgA Fc domains to the cognate Fc receptor CD89 (FcalphaRI), and IgE domains to cognate Fc receptors FcER1 and CD23. 

Monoclonal antibodies can be derived from B cells.

Interaction of B cells with T cells

Once an activated TH cell (one that has interacted with an antigen-class II MHC complex on a macrophage) recognizes a processed antigen displayed by a class II MHC molecule on the membrane of a B cell, the 2 cells interact. The TH cells in these conjugates undergo reorganization of the Golgi apparatus and microtubular organizing center as well as clustering of several membrane proteins near the junction of the 2 cells. This aids in the directional release of cytokines from the TH cell toward the interacting B cell. Both IL-1 and IL-4 function as activation signals.

B Cell Markers

Examples of B cell surface markers include CD10, CD19, CD20, CD21, CD22, CD23, CD24, CD37, CD53, CD72, CD74, CD75, CD77, CD79a, CD79b, CD80, CD81, CD82, CD83, CD84, CD85, CD86. B cell surface markers have been suggested as targets for the treatment of B cell disorders, autoimmune disease, and transplantation rejection. Antibodies that specifically bind these markers have also been developed.

CD20: Antibody based therapies directed against CD20 has been shown to be an effective in vivo treatment for non-Hdogkin’s lymphoma and partially effective in attenuating the manifestations of rheumatoid arthritis, SLE, idiopathic thrombocytopenic purpura and hemolytic anemai.

CD22: Anti-CD22 antibodies have been used in the treatment of non-Hodkin’s lymphoma (Renner, Leukemia 1997, S5509), the treatment of autoimmune disorders (US2003/0202975), the treatment of lymphomas and leukemia (US 2004/0001828) and cancer (US 5,789,554).