B lymphocytes and systemic lupus erythematosus
- Cite this article as:
- Criscione, L.G. & Pisetsky, D.S. Curr Rheumatol Rep (2003) 5: 264. doi:10.1007/s11926-003-0004-x
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Systemic lupus erythematosus (SLE) is a prototypic autoim-mune disease characterized by B cell hyperactivity in associa-tion with autoantibodies, most prominently those directed to components of the cell nucleus. The source of the antigens that drive B cell responses in SLE is unknown, although recent studies suggest mechanisms by which the self-antigens become immunogenic and stimulate responses. Among these mecha-nisms, abnormalities in the generation of apoptotic cells or their clearance may increase the availability of nuclear antigens to drive responses. In addition, autoantibody crossreactivity may promote induction of responses to disparate antigens, foreign and self, and enable a single autoantibody to cause dis-ease by crossreactive binding. In addition to reflecting increased exposure to self-antigen, autoantibody responses in SLE may result from abnormalities in B cell signaling and regu-lation by cytokines. New approaches to therapy aim to abro-gate autoantibody production by targeting specific steps in B cell activation, including blockade of T cell costimulation.