The preferential accumulation of helper‐inducer T lymphocytes in inflammatory lesions: evidence for regulation by selective endothelial and homotypic adhesion

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Abstract
The mechanisms which lead to the accumulation of T lymphocytes into inflammatory lesions are not clearly understood. We have previously shown that synovial CD4 T lymphocytes are mostly CDw29UCHL1 (helper-inducer cells) and very few carry the CD45R antigen which identifies the suppressor-inducer subset. Synovial CD8 cells are also CDw29UCHL1CD45R−. In the present study, lymphocytes from pleural and peritoneal inflammatory infiltrates were shown to have a similar phenotypic pattern. Furthermore, it was demonstrated that the CDw29UCHL1 subset had a greater ability than CD45R cells to adhere to endothelial cells and to form homotypic clusters. Differential surface expression of LFA-1 on the two subsets was also shown, but this could not account for the demonstrated adhesion differences. Differences in adhesion between CDw29/UCHL1 and CD45R cells may explain the preferential accumulation of CDw29/UCHL1 cells in inflammatory infiltrates and underlie some of the functional differences between cells taken from sites of chronic inflammation and those from peripheral blood.

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