tailieunhanh - Báo cáo y học: "Apolipoprotein A-I infiltration in rheumatoid arthritis synovial tissue: a control mechanism of cytokine production"

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: Apolipoprotein A-I infiltration in rheumatoid arthritis synovial tissue: a control mechanism of cytokine production? | Available online http content 6 6 R563 Research article Apolipoprotein A-I infiltration in rheumatoid arthritis synovial tissue a control mechanism of cytokine production Barry Bresnihan 1 Martina Gogarty1 Oliver FitzGerald1 Jean-Michel Dayer2 and Danielle Burger2 Department of Rheumatology St Vincents University Hospital Dublin Ireland 2Service of Immunology and Allergy Faculty of Medicine Geneva Switzerland Corresponding author Danielle Burger Received 22 Jun 2004 Accepted 1 9 Aug 2004 Published 6 Oct 2004 Arthritis Res Ther 2004 6 R563-R566 DOI ar1443 2004 Bresnihan 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 cited. Open Access Abstract The production of tumor necrosis factor a TNF-a and interleukin-1 p IL-1P by monocytes is strongly induced by direct contact with stimulated T lymphocytes and this mechanism may be critical in the pathogenesis of rheumatoid arthritis RA . Apolipoprotein A-I apoA-I blocks contact-mediated activation of monocytes causing inhibition of TNF-a and IL-1 p production. This study examined the hypothesis that apoA-I may have a regulatory role at sites of macrophage activation by T lymphocytes in inflamed RA synovial tissue. Synovial tissue samples were obtained after arthroscopy from patients with early untreated RA or treated RA and from normal subjects. As determined by immunohistochemistry apoA-I was consistently present in inflamed synovial tissue that contained infiltrating T cells and macrophages but it was absent from noninflamed tissue samples obtained from treated patients and from normal subjects. ApoA-I staining was abundant in the perivascular areas and extended in a halo-like pattern to the surrounding cellular infiltrate. C-reactive