Contribution of B-1a cells to systemic lupus erythematosus in the NZM2410 mouse model
- PMID: 25728381
- PMCID: PMC4550580
- DOI: 10.1111/nyas.12607
Contribution of B-1a cells to systemic lupus erythematosus in the NZM2410 mouse model
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.
Keywords: B-1a cell; NZM2410 mice; systemic lupus erythematosus.
© 2015 New York Academy of Sciences.
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