Innate immunity triggers IL-32 expression by fibroblast-like synoviocytes in rheumatoid arthritis |
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| Authors: | Ghada Alsaleh Laetitia Sparsa Emmanuel Chatelus Mathieu Ehlinger Jacques-Eric Gottenberg Dominique Wachsmann Jean Sibilia |
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| Institution: | 1.EA3948, Laboratoire Physiopathologie des Arthrites, Université de Strasbourg, UFR Sciences Pharmaceutiques, 74 route du Rhin, 67401 Illkirch, France;2.Département de Rhumatologie, Hôpitaux Universitaires de Strasbourg, avenue Molière, Strasbourg Hautepierre 67200, France;3.Département d''Orthopédie, Hôpitaux Universitaires de Strasbourg, Strasbourg Hautepierre 67200, France |
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| Abstract: | Introduction Interleukin-32 (IL-32) is a recently described cytokine that is a strong inducer of pro-inflammatory cytokines such as tumor
necrosis factor (TNF)-α, IL-1β, IL-6, and IL-8. The expression of this cytokine is highly increased in the rheumatoid synovium
and correlated with the severity of joint inflammation. Little is known regarding the innate immune-related regulation of
IL-32 by fibroblast-like synoviocytes (FLSs). We therefore investigated the effect of innate immune stimulation by ligands
of Toll-like receptor (TLR)2, TLR3, and TLR4, and cytokines such as TNF-α and interferon (IFN)-γ, on IL-32 expression by FLSs. |
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