Contribution of B-1a cells to systemic lupus erythematosus in the NZM2410 mouse model.
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.
Department of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, Florida.
Zhiwei
Z
Xu
Department of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, Florida.
Laurence
L
Morel
D000818:Animals; D016175:B-Lymphocyte Subsets / Q000502:physiology*; D050763:Cyclin-Dependent Kinase Inhibitor p18 / Q000172:deficiency* / Q000235:genetics*; D004195:Disease Models, Animal; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000235:genetics* / Q000276:immunology / Q000378:metabolism*; D051379:Mice
C493972:Cdkn2c protein, mouse; D050763:Cyclin-Dependent Kinase Inhibitor p18
B-1a cell; NZM2410 mice; systemic lupus erythematosus