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Contribution of B‐1a cells to systemic lupus erythematosus in the NZM2410 mouse model
Author(s) -
Xu Zhiwei,
Morel Laurence
Publication year - 2015
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.12607
Subject(s) - autoantibody , immunology , pathogenesis , effector , b cell , systemic lupus erythematosus , autoimmune disease , lupus erythematosus , etiology , biology , medicine , disease , pathology , antibody
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.