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IL-17 Promotes Murine Lupus
Author(s) -
Gil Amarilyo,
Elaine Lourenço,
FuDong Shi,
Antonio La Cava
Publication year - 2014
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.1400931
Subject(s) - pathogenesis , immunology , systemic lupus erythematosus , lupus nephritis , autoantibody , proinflammatory cytokine , cd8 , blockade , interleukin 17 , autoimmunity , lupus erythematosus , medicine , biology , inflammation , immune system , receptor , antibody , disease
The proinflammatory activity of IL-17-producing Th17 cells has been associated with the pathogenesis of several autoimmune diseases. In this article, we provide direct evidence for a role of IL-17 in the pathogenesis of systemic lupus erythematosus (SLE). The induction of SLE by pristane in IL-17-sufficient wild-type mice did not occur in IL-17-deficient mice, which were protected from development of lupus autoantibodies and glomerulonephritis. The protection from SLE in IL-17-deficient mice was associated with a reduced frequency of CD3(+)CD4(-)CD8(-) double-negative T cells and an expansion of CD4(+) regulatory T cells, and did not depend on Stat-1 signaling. These data affirm the key role of IL-17 in the pathogenesis of SLE and strengthen the support for IL-17 blockade in the therapy of SLE.

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