B cells as effectors and regulators of autoimmunity

Abstract

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.

Keywords::

• B cells
• autoimmune
• type 1 diabetes
• NOD mouse
• T cells

Declaration of interest: We thank Dr. Pablo Silveira and Ms. Stacey Walters for proofreading the manuscript and insightful comments and discussion. The authors declare that there are no financial, consulting, nor personal relationships with other people or organizations that could influence the author's work. E.M. is supported by a National Health Medical Research (NHMRC) Dora Lush Scholarship and the Ross Trust. S.T.G. is an Australian Research Council Future Fellow and an Honorary NHMRC Research Fellow. E.M. and S.T.G. conducted the literature review, discussed data and co-wrote the manuscript.