Journal
CRITICAL REVIEWS IN IMMUNOLOGY
Volume 36, Issue 6, Pages 485-509Publisher
BEGELL HOUSE INC
DOI: 10.1615/CritRevImmunol.2017020284
Keywords
systemic lupus erythematosus; autoantibodies; Ets1; B-cell tolerance; plasma cells; T-cell cytokines
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Funding
- National Institutes of Health [AI122720]
- Lupus Research Alliance
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI122720] Funding Source: NIH RePORTER
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Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by excess B- and T-cell activation, the development of autoantibodies against self-antigens including nuclear antigens, and immune complex deposition in target organs, which triggers an inflammatory response and tissue damage. The genetic and environmental factors that contribute to the development of SLE have been studied extensively in both humans and mouse models of the disease. One of the important genetic contributions to SLE development is an alteration in the expression of the transcription factor Ets1, which regulates the functional differentiation of lymphocytes. Here, we review the genetic, biochemical, and immunological studies that have linked low levels of Ets1 to aberrant lymphocyte differentiation and to the pathogenesis of SLE.
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