Arthritis & Rheumatism, Volume 63,
November 2011 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Chicago, Illinois November 4-9, 2011.


The Role of IL-17 in Systemic Lupus Erythematosus.

Amarilyo1,  Gil, Lourenco2,  Elaine, La Cava3,  Antonio

University of California, Los Angeles, Los Angeles, CA
UCLA David Geffen School of Medicine, Los Angeles, CA
Univ of California Los Angeles, Los Angeles, CA

Background/Purpose:

T helper 17 cells (Th17), named after their signature cytokine IL-17, favor the development and progression of autoimmune diseases such as rheumatoid arthritis, Crohn's disease and multiple sclerosis. A role for Th17 cells in systemic lupus erythematosus (SLE) has been suggested by the finding that sera from lupus patients had abnormally elevated levels of IL-17 that correlated with disease activity, and by the observation that IL-17-producing T cells were present in kidney infiltrates of murine models as well as patients with lupus nephritis. Here we studied the role of IL-17 in the development of lupus-like disease induced by pristane in mice.

Methods:

IL-17 knockout mice (on the B6 background) were compared with wild-type B6 mice (WT) for the development of lupus-like disease after intraperitoneal injection of the hydrocarbon oil pristane (which induces a lupus-like disease characterized by the development of lupus-associated autoantibodies and glomerulonephritis). Total and percentage numbers of peripheral CD4, CD8 and related subsets including CD4+CD25+Foxp3+ regulatory T cells (Treg) were monitored ex vivo by flow cytometry at time 0, 3 weeks, 3 months, 5 months and 8 moths after disease induction in IL-17 knockout mice as compared to WT control mice.

Results:

IL-17 deficient mice treated with pristane had reduced hypergammaglobulinemia and lower levels of anti-ssDNA and anti-chromatin antibodies in comparison with WT mice treated with pristane. The onset and the extent of glomerulonephritis were also delayed in the IL-17-deficient mice. Although IL-17 deficient mice had similar levels of CD4 and CD8 when compared to pristane injected wild type mice, they had significantly higher numbers of Treg by three months after pristane injection (p<0.003), and this number subsequently declined.

Conclusion:

IL-17 deficiency reduced the development of lupus-like disease induced by pristane. These findings suggest a direct role of Il-17 in the SLE pathogenesis and may point towards a new drug therapy pathway for this disease.

To cite this abstract, please use the following information:
Amarilyo, Gil, Lourenco, Elaine, La Cava, Antonio; The Role of IL-17 in Systemic Lupus Erythematosus. [abstract]. Arthritis Rheum 2011;63 Suppl 10 :1831
DOI:

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