B lymphocytes and systemic lupus erythematosus.

Journal Article (Review)

Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by B cell hyperactivity in association 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 mechanisms, 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 disease 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 regulation by cytokines. New approaches to therapy aim to abrogate autoantibody production by targeting specific steps in B cell activation, including blockade of T cell costimulation.

Full Text

Duke Authors

Cited Authors

  • Criscione, LG; Pisetsky, DS

Published Date

  • August 2003

Published In

Volume / Issue

  • 5 / 4

Start / End Page

  • 264 - 269

PubMed ID

  • 14531953

International Standard Serial Number (ISSN)

  • 1523-3774

Language

  • eng

Conference Location

  • United States