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Role of adhesion molecules in the lymphoid cell distribution in rheumatoid synovial membrane

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Summary

We studied the staining pattern of a group of adhesion molecules in the lining layer and lymphocytic infiltrates of the rheumatoid synovial membrane, using monoclonal antibodies against lymphocyte function associated antigen-1 (LFA-1), very late activation antigen-4 (VLA-4), VLA-5, endothelial leucocyte adhesion molecule-1 (ELAM-1) and intercellular adhesion molecule-1 (ICAM-1). The cells of the the lining layer were strongly ICMA-1 positive and VLA-5 positive, suggesting (1) that ICAM-1 may function to facilitate the adhesion of ICAM-1-bearing type A cells to type B lining cells and (2) that the lining cells may utilize VLA-5 for anchorage to fibronectin at the surface of the synovial membrane. In the lymphocyte-rich and transitional areas, the endothelial cells of the postcapillary venules were both ELAM-1 positive and ICAM-1 positive. ICAM-1 staining was weak in lymphoid aggregates, but strong in the transitional areas, indicating a paucity of ICAM-1-bearing cells in the lymphocyte-rich areas. On the other hand, LFA-1 staining was very strong in the lymphoid aggregates and only moderate in transitional areas. This suggested that the large numbers of T4 cells present in the lymphocyte-rich areas are sufficiently activated to express substantial levels of LFA-1, and also that the LFA-1 molecule is an important receptor for emigration from postcapillary venules. In germinal centre like areas in lymphoid aggregates, most of the cells stained strongly for ICAM-1 and VLA-4, suggesting that the proliferation of B lymphocytes may be facilitated by LFA-1- and VLA4-dependent T and B cell interaction. The VLA molecules stained in the transitional areas may provide appropriate adhesion and anchorage of lymphocytes for the achievement of the variety of immune reactions in which these cells are engaged in these areas.

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Ishikawa, H., Hirata, S., Nishibayashi, Y. et al. Role of adhesion molecules in the lymphoid cell distribution in rheumatoid synovial membrane. Rheumatol Int 13, 229–236 (1994). https://doi.org/10.1007/BF00290200

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