IL-17 and the Th17 lineage in systemic lupus erythematosus.
OBJECTIVE
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.


RESULTS
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.


CONCLUSIONS
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.
Garrett-Sinha
Lee Ann
LA
Department of Biochemistry, School of Medicine and Biomedical Sciences, The University at Buffalo, State University of New York, Buffalo, New York 14203, USA. leesinha@buffalo.edu
John
Shinu
S
Gaffen
Sarah L
SL
D000818:Animals; D015551:Autoimmunity / Q000276:immunology*; D019070:Cell Lineage / Q000276:immunology*; D006801:Humans; D020381:Interleukin-17 / Q000276:immunology*; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology*
D020381:Interleukin-17