Why do B cells mutate their immunoglobulin receptors?

• Published in: Trends in Immunology Vol. 27; no. 8; pp. 374 - 380
• Main Authors: Longo, Nancy S., Lipsky, Peter E.
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.08.2006; Elsevier Limited
• Subjects: Antibodies - immunology; Antibody Affinity; B-Lymphocytes - immunology; Binding sites; Genes, Immunoglobulin - immunology; HIV; Human immunodeficiency virus; Humans; Immune system; Immunologic Memory; Influenza; Microorganisms; Models, Immunological; Mutation; Receptors, Antigen, B-Cell - immunology; Somatic Hypermutation, Immunoglobulin; Vertebrates
• ISSN: 1471-4906; 1471-4981; 1365-2567
• DOI: 10.1016/j.it.2006.06.007

B cells have the unique ability to acquire large numbers of point mutations in the variable segment of rearranged immunoglobulin (Ig) genes during a germinal center reaction. It is broadly accepted that somatic hypermutation (SHM) and affinity maturation are required to generate memory B cells and to produce antibodies capable of accomplishing the host defense functions of the humoral component of the adaptive immune system. However, several studies illustrate that low-avidity interactions between antigen and the B-cell receptor can induce deletion, receptor editing and a T-dependent immune response, suggesting that the high-avidity binding of antigen is not essential. If enhanced antigen binding is not essential for immune responses, what is the purpose of SHM? An alternative benefit of SHM might be to enhance the ability of B cells to track antigens expressed by rapidly mutating microorganisms.