An Immunohistochemical and Immunoelectron Microscopic Study of Adhesion Molecules in Synovial Pannus Formation in Rheumatoid arthritis

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To investigate the mechanism of synovial-pannus formation in rheumatoid arthritis, using immunohistochemical and immunoelectron microscopic studies with monoclonal antibodies against the adhesion molecules, anti-CD54 (ICAM-1) anti-CD11a (LFA-1), anti-CDw49a (VLA-1), anti-CDw49b (VLA-2), anti-CDw49c (VLA-3), anti-CDw49d (VLA-4) and anti-CDw49e (VLA-5), the pattern of distribution of these molecules at the rheumatoid synovial-cartilage junction have been investigated. Treatment with anti-ICAM-1 resulted in membrane staining of most of the macrophages and fibroblasts infiltrating the synovial tissue and bordering the pannus cartilage junction. This suggests the possibility that ICAM-1 may function to facilitate the adhesion of Type A cells bearing ICAM-1 to Type B cells. ICAM-1 positive macrophages and fibroblasts were often in contact with lymphoid cells also suggest that cell-to-cell immune reaction occurs in the formation of the pannus. Our present study shows that VLA-3, VLA-4 and particularly VLA-5 are the predominant β1 integrins expressed by rheumatoid synovial pannus. Since these three integrins all function as fibronectin receptors, it is tempting to postulate that the fibronectin rich environment of the rheumatoid cartilage surface could effectively trap pannus cells expressing high levels of these molecules. VLA-5 molecule found in pericellular and interterritorial matrix distribution in the present study strongly suggests that receptor-ligand interaction between VLA-5 and cartilage matrix may occur at the early stage of pannus formation. Furthermore, the increase in β1 integrin may be necessary for the growth of the pannus and also for the upregulation of the VLA-molecules, leading secondarily to increase attachment.

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