Journal
CURRENT OPINION IN RHEUMATOLOGY
Volume 20, Issue 5, Pages 519-525Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/BOR.0b013e328304b6b5
Keywords
chemokines; interleukin-17; lupus; mouse model; Th17
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Funding
- NIAID NIH HHS [AI49329] Funding Source: Medline
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Purpose of review Systemic lupus erythematosus etiology includes both genetic and environmental factors. Evidence suggests that many genetic loci in humans and mouse models contribute to the occurrence and clinical presentation of lupus. This large array of different genes affects many aspects of immune cell function, including the activation and functional differentiation of B cells, T cells, dendritic cells and other immune cells. In particular, the T-cell components that contribute to systemic lupus erythematosus pathogenesis are incompletely defined. Recent findings A major paradigm shift in understanding how CD4(+) T cells contribute to autoimmunity recently occurred with the discovery of a new T-cell population that produces the cytokine IL-17 (IL-17A), termed 'Th17'. Although Th17 cells contribute to autoimmune disease in rheumatoid arthritis and Crohn's disease, their role in systemic lupus erythematosus is far less clear. Summary In this review, we focus on an emerging role for the cytokine IL-17 and the cells that produce it in contributing to lupus in particular based on recent findings in animal models.
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