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Review
. 2015 Dec;1362(1):215-23.
doi: 10.1111/nyas.12607. Epub 2015 Feb 26.

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

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Review

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

Zhiwei Xu et al. Ann N Y Acad Sci. 2015 Dec.

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.

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Figures

Figure 1
Figure 1
Proposed model for the p18 regulation of autoimmune pathogenesis in the NZM2410 model of lupus. Boxes show processes that we have observed in the experiments reviewed here. Filled arrows shown causal links established by our studies or that of others. Dashed arrows show potential causal links based on either in vitro studies and/or associations.

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