THE ROLE OF ADHESION MOLECULES IN THE PATHOGENESIS OF RHEUMATOID-ARTHRITIS

被引：36

作者：

POSTIGO, AA ^{[1
]}

GARCIAVICUNA, R ^{[1
]}

LAFFON, A ^{[1
]}

SANCHEZMADRID, F ^{[1
]}

机构：

[1] UNIV AUTONOMA MADRID,HOSP PRINCESA,SERV INMUNOL,C DIEGO LEON 62,E-28006 MADRID,SPAIN

来源：

AUTOIMMUNITY | 1993年 / 16卷 / 01期

关键词：

RHEUMATOID ARTHRITIS; T-CELL ADHESION; ENDOTHELIUM; INTEGRINS; SELECTINS CD44;

D O I：

10.3109/08916939309010649

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

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.

引用

页码：69 / 76

页数：8

共 64 条

[1] Harris E.D., Rheumatoid arthritis. Pathophysiology and implications for therapy, N Eng J Med, 322, pp. 1277-1289, (1990)
[2] Panayi G.S., Lanchbury J.S., Kingsley G.H., The importance of the T cell in initiating and maintaining the chronic synovitis of rheumatoid arthritis, Arthritis Rheum, 35, pp. 722-729, (1992)
[3] Firestein G.S., Zvaifler N.J., How important are T cells in chronic inflammatory synovitis?, Arthritis Rheum, 37, pp. 768-773, (1990)
[4] van Eden W., Holoshitz J., Nevo Z., Frenkel A., Klajman A., Cohen I.R., Arthritis induced by a T lymphocyte clone that responds to mycobacterium, Proc Natl Acad Sci USA, 82, pp. 5117-5120, (1985)
[5] Holoshitz J., Matitiau A., Cohen I.R., Arthritis induced in rats by cloned T lymphocytes responsive to mycobacteria, J Clin Invest, 73, pp. 211-215, (1984)
[6] Yu D.T.Y., Winchester R.J., Ru S.M., Gibofsky A., Ko H.S., Kunkel H.J., Peripheral blood la positive cells. Increases in certain diseases after immunization, J Exp Med, 151, pp. 91-101, (1980)
[7] Shimizu Y., Newman W., Tanaka Y., Shaw S., Lymphocyte interactions with endothelial cells, Immunol Today, 13, pp. 106-112, (1992)
[8] Hynes R.O., Integrins: Versatility, modulation, and signaling in cell adhesion, Cell, 69, pp. 11-25, (1992)
[9] Mackay C.R., Marston W.L., Dudler L., Naive and memory T cells show distinct pathways of lymphocyte recirculation, J Exp Med, 171, pp. 801-807, (1990)
[10] Sanders M.E., Makgoba M.W., Sharrow S.O., Stephany D., Springer T.A., Young H.A., Shaw S., Human memory T lymphocytes express increased levels of three cell adhesion molecules (LFA-3, CD2, and LFA-1) and three other molecules (UCHL-1, CDw29, and Pgp-1) and have enhanced IFN gamma production, J Immunol, 140, pp. 1401-1407, (1988)

← 1 2 3 4 5 6 7 →