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:Polarized subsets of human T-helper cells induce distinct patterns of chemokine production by normal and systemic sclerosis dermal fibroblasts. | Available online http content 8 1 R10 Research article Polarized subsets of human T-helper cells induce distinct patterns of chemokine production by normal and systemic sclerosis dermal fibroblasts Carlo Chizzolini1 Yann Parel1 Agneta Scheja2 and Jean-Michel Dayer1 Immunology and Allergy Geneva University Hospital Geneva School of Medicine Rue Micheli-du-Crest 24 1211 Geneva 14 Switzerland 2Division of Rheumatology Lund University Hospital 221 85 Lund Sweden Corresponding author Carlo Chizzolini chizzolini@ Received 25 Jun 2005 Revisions requested 14 Jul 2005 Revisions received 10 Oct 2005 Accepted 3 Nov 2005 Published 30 Nov 2005 Arthritis Research Therapy 2006 8 R10 doi ar1 860 This article is online at http content 8 1 R1 0 2005 Chizzolini 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 The role of fibroblasts in inflammatory processes and their cross-talk with T cells is increasingly being recognized. Our aim was to explore the capacity of dermal fibroblasts to produce inflammatory chemokines potentially involved in fibrosis occurring in response to contact with polarized human T cells. Our findings indicate that the program of chemokine production by fibroblasts is differentially regulated depending on the T-helper Th cell subset used to activate them. Thus Th1 and Th2 cells preferentially induced production of IFN-y inducible protein IP -10 and IL-8 respectively whereas monocyte chemoattractant protein MCP -1 was equally induced by both subsets at mRNA and protein levels. Neutralization experiments indicated that membrane-associated tumour necrosis factor-a and IL-1 played a major role in the induction of IL-8 and MCP-1
