The role of Adhesion Molecules in the Pathogenesis of Rheumatoid Arthritis
作者:
PostigoAntonio A.,
GarciaRosario,
LaffónArmando,
SánchezFrancisco,
期刊:
Autoimmunity
(Taylor Available online 1993)
卷期:
Volume 16,
issue 1
页码: 69-76
ISSN:0891-6934
年代: 1993
DOI:10.3109/08916939309010649
出版商: Taylor&Francis
关键词: Rheumatoid Arthritis;T cell adhesion;Endothelium;Integrins;Selectins CD44
数据来源: Taylor
摘要:
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by infiltration of mononuclear cells, mainly T lymphocytes, into the synovial membrane (SM). The interaction of peripheral blood T cells with the different components of the rheumatoid synovium is mediated by cell surface proteins such as selectins, integrins, members of the immunoglobulin superfamily and homing receptors. T lymphocytes infiltrating the rheumatoid SM show an activated phenotype and display an increased avidity of their adhesion receptors that results in an enhanced interaction of these cells with both extracellular matrix proteins (ECM) and cellular ligands (VCAM-1, ICAMs). The interaction of T cell integrins with their ligands, besides an additional antigenic stimulus, could trigger a mitogenic response on these cells, a phenomenon that can contribute to increased cellularity observed into the rheumatoid SM. Moreover, cell attachment to ECM through integrins induces the secretion of several proteases that can contribute to the tissue damage observed in RA. The increased knowledge about the role of adhesion receptors in the pathogenesis of RA and other inflammatory diseases will allow the introduction of a new therapeutic approach by: the use of specific blocking reagents designed to interfere with the function of adhesion molecules.
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