tailieunhanh - Báo cáo y học: "Interactions between IL-32 and tumor necrosis factor alpha contribute to the exacerbation of immune-inflammatory diseases"

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: Interactions between IL-32 and tumor necrosis factor alpha contribute to the exacerbation of immune-inflammatory diseases. | Available online http content 8 6 R166 Research article Interactions between IL-32 and tumor necrosis factor alpha contribute to the exacerbation of immune-inflammatory diseases Hirofumi Shoda1 Keishi Fujio1 Yumi Yamaguchi1 Akiko Okamoto1 Tetsuji Sawada1 Yuta Kochi2 and Kazuhiko Yamamoto1 Department of Allergy and Rheumatology Graduate School of Medicine University of Tokyo 7-3-1 Hongo Bunkyo-ku Tokyo 113-0033 Japan 2Laboratory for Rheumatic Diseases SNP Research Center RIKEN 1-7-22 Suehiro-cho Tsurumi-ku Yokohama Kanagawa 230-0045 Japan Corresponding author Keishi Fujio kfujio-tky@ Received 12 Jul 2006 Revisions requested 3 Aug 2006 Revisions received 5 Oct 2006 Accepted 1 Nov 2006 Published 1 Nov 2006 Arthritis Research Therapy 2006 8 R166 doi ar2074 This article is online at http content 8 6 R166 2006 Shoda et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Open Access Abstract IL-32 is a newly described cytokine in the human found to be an in vitro inducer of tumor necrosis factor alpha TNFa . We examined the in vivo relationship between IL-32 and TNFa and the pathologic role of IL-32 in the TNFa-related diseases -arthritis and colitis. We demonstrated by quantitative PCR assay that IL-32 mRNA was expressed in the lymphoid tissues and in stimulated peripheral T cells monocytes and B cells. Activated T cells were important for IL-32 mRNA expression in monocytes and B cells. Interestingly TNFa reciprocally induced IL-32 mRNA expression in T cells monocyte-derived dendritic cells and synovial fibroblasts. Moreover IL-32 mRNA expression was prominent in the synovial tissues of rheumatoid arthritis patients especially in synovial-infiltrated lymphocytes by .