Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Innate immunity triggers IL-32 expression by fibroblast-like synoviocytes in rheumatoid arthritis. | Alsaleh et al. Arthritis Research Therapy 2010 12 R135 http content 12 4 R135 RESEARCH ARTICLE Open Access Innate immunity triggers IL-32 expression by fibroblast-like synoviocytes in rheumatoid arthritis Ghada Alsaleh 1 2 Laetitia Sparse11 2 Emmanuel Chatelus 1 2 Mathieu Ehlinger3 Jacques-Eric Gottenberg1 2 Dominique Wachsmann 1 2 and Jean Sibilia1 2 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 -a IL-1P 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-a and interferon IFN -y on IL-32 expression by FLSs. Methods FLSs were isolated from patients with rheumatoid arthritis RA according to the ACR criteria. Quantitative RT-PCR confocal analysis and ELISA were performed to evaluate IL-32 mRNA induction and IL-32 release by FLSs stimulated with TLR2 BLP TLR3 poly I C and TLR4 lipopolysaccharide ligands TNF-a and IFN-y. Results TLR2 -3 and -4 ligands as well as IFN-Y and TNF-a induced IL-32 p Y and Ỗ mRNA expression by RA FLSs. Mature IL-32 was expressed intracellularly and released by cells stimulated with the various activators. The IL-32a isoform was expressed intracellularly in response to TNF-a and poly I C and not released in culture supernatants. Stimulation of FLS with TNF-a BLP lipopolysaccharide or poly I C concomitant with IFN-Y increased IL-32 expression compared with stimulation with IFN-Y alone. Conclusions IL-32 synthesis by FLSs is tightly regulated by innate immunity in rheumatoid arthritis. Thus TNF-a IFN-Y double-strand RNA hyaluronic acid or other .