Autoantibody-dependent and autoantibody-independent roles for B cells in systemic lupus erythematosus: Past, present, and future

Abstract

It has long been known that B cells produce autoantibodies and, thereby, contribute to the pathogenesis of many autoimmune diseases. Systemic lupus erythematosus (SLE), a prototypic systemic autoimmune disorder, is characterized by high-circulating autoantibody titers and immune-complex deposition that can trigger inflammatory damage in multiple organs/organ systems. Although the interest in B cells in SLE has historically focused on their autoantibody production, we now appreciate that B cells have multiple autoantibody-independent roles in SLE as well. B cells can efficiently present antigen and activate T cells, they can augment T cell activation through co-stimulatory interactions, and they can produce numerous cytokines which affect inflammation, lymphogenesis, and immune regulation. Not surprisingly, B cells have become attractive therapeutic targets in SLE. With these points in mind, this review will focus on the autoantibody-dependent and autoantibody-independent roles for B cells in SLE and on therapeutic approaches that target B cells.

Keywords::

• Antigen presentation
• autoantibodies
• B cells
• co-stimulation
• cytokines
• systemic lupus erythematosus

Declaration of interest: This work was supported in part by NIH grant R01 AR050193 (WS) and an American College of Rheumatology Research and Education Foundation Abbott Medical Student Clinical Preceptorship Award (NJ). The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.