Contribution of B‐1a cells to systemic lupus erythematosus in the NZM2410 mouse model. Issue 1 (26th February 2015)

• Record Type: Journal Article
• Authors: Xu, Zhiwei; Morel, Laurence
• Other Names: Rothstein Thomas L. guestEditor.; Herzenberg Leonore A. guestEditor.; Holodick Nichol E. guestEditor.; Ghosn Eliver guestEditor.
• Is Part Of: Annals of the New York Academy of Sciences. Volume 1362:Issue 1(2015)
• Page Start: 215
• Page End: 223
• Publication Date: 2015-02-26
• Subjects: systemic lupus erythematosus -- B‐1a cell -- NZM2410 mice; Medical sciences -- Periodicals; Medicine -- Periodicals; Science -- Periodicals; 610
• DOI: 10.1111/nyas.12607
• Languages: English
• ISSNs: 0077-8923

Abstract

Abstract : Systemic lupus erythematosus (SLE) is an autoimmune disease of complex etiology in which B cells play a central role. An expanded number of B‐1a cells have been consistently associated with murine lupus, and more recently with human SLE. We have identified Cdkn2c, a gene that controls cell cycle progression, as a key regulator of B‐1a cell numbers and have associated Cdkn2c deficiency with autoimmune pathology, including the production of autoantibodies and the skewing of CD4 + T cells toward inflammatory effector functions. We review the genetic studies that have led to these findings, as well as the possible mechanisms by which B‐1a cell expansion and Cdkn2c deficiency are related to SLE pathogenesis.