TAILIEUCHUNG - Báo cáo y học: "Innate immunity triggers IL-32 expression by fibroblast-like synoviocytes in rheumatoid arthritis"

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 .

TỪ KHÓA LIÊN QUAN
Đã phát hiện trình chặn quảng cáo AdBlock
Trang web này phụ thuộc vào doanh thu từ số lần hiển thị quảng cáo để tồn tại. Vui lòng tắt trình chặn quảng cáo của bạn hoặc tạm dừng tính năng chặn quảng cáo cho trang web này.