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- W1569272321 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." @default.
- W1569272321 created "2016-06-24" @default.
- W1569272321 creator A5002019326 @default.
- W1569272321 creator A5026532447 @default.
- W1569272321 date "2015-02-26" @default.
- W1569272321 modified "2023-10-02" @default.
- W1569272321 title "Contribution of B‐1a cells to systemic lupus erythematosus in the NZM2410 mouse model" @default.
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- W1569272321 doi "https://doi.org/10.1111/nyas.12607" @default.
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- W1569272321 hasPublicationYear "2015" @default.
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