Contribution of B-1a cells to systemic lupus erythematosus in the NZM2410 mouse model

Zhiwei Xu, Laurence Morel

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)215-223
Number of pages9
JournalAnnals of the New York Academy of Sciences
Volume1362
Issue number1
DOIs
StatePublished - Dec 1 2015
Externally publishedYes

Keywords

  • B-1a cell
  • NZM2410 mice
  • Systemic lupus erythematosus

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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