B cells as effectors and regulators of autoimmunity

• Published in: Autoimmunity (Chur, Switzerland) Vol. 45; no. 5; pp. 377 - 387
• Main Authors: Mariño, Eliana, Grey, Shane T.
• Format: Journal Article
• Language: English
• Published: England Informa Healthcare 01-08-2012; Taylor & Francis
• Subjects: Animals; Antigen-Presenting Cells - immunology; Antigen-Presenting Cells - metabolism; Autoantibodies - immunology; autoimmune; Autoimmunity - immunology; B cells; B-Lymphocytes - immunology; B-Lymphocytes - metabolism; B-Lymphocytes, Regulatory - immunology; CD4-Positive T-Lymphocytes - immunology; CD8-Positive T-Lymphocytes - immunology; Cell Communication - immunology; Cytokines - biosynthesis; Cytokines - immunology; Diabetes Mellitus, Type 1 - immunology; Diabetes Mellitus, Type 1 - metabolism; Disease Models, Animal; Epitopes - immunology; Epitopes - metabolism; Humans; Immune Tolerance; Lymphocyte Depletion; Mice; Mice, Inbred NOD; NOD mouse; T cells; T-Lymphocytes, Regulatory - immunology; type 1 diabetes
• ISSN: 0891-6934; 1607-842X
• DOI: 10.3109/08916934.2012.665527

A classic understanding of the interplay between B and T cell components of the immune system that drive autoimmunity, where B cells provide an effector function, is represented by systemic lupus erythematosus (SLE), an autoimmune condition characterised by the production of auto-antibodies. In SLE, CD4+T cells provide cognate help to self-reactive B cells, which in turn produce pathogenic auto-antibodies (1). Thus, B cells act as effectors by producing auto-antibody aided by T cell help such that B and T cell interactions are unidirectional. However, this paradigm of B and T cell interactions is challenged by new clinical data demonstrating that B cell depletion is effective for T cell mediated autoimmune diseases including type I diabetes mellitus (T1D) (2), rheumatoid arthritis (3), and multiple sclerosis (4). These clinical data indicate a model whereby B cells can influence the developing autoimmune T cell response, and therefore act as effectors, in ways that extend beyond the production of autoantibody (5). In this review by largely focusing on type I diabetes we will develop a hypothesis that bi-directional B and T interactions control the course of autoimmunity.