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An CD11a/CD18-dependent homotypic aggregation pathway is induced by triggering CD45 molecules on human thymocytes. By contrast, a CD11a/CD18-independent homotypic aggregation process is induced by triggering the CD99 molecule (E2, MIC2 gene product) expressed at the surface of either Jurkat T cells or human thymocytes. A new quantitative method based on FACS analysis of aggregated cells was used and allowed to show that both types of aggregation (CD11a/CD18-dependent and CD11a/CD18-independent) were inhibited with sphingosine, oleylamine or stearylamine. These three compounds had no effect on the expression of CD99, CD45, CD11a, CD18 or other [correction of others] known integrins expressed at the surface of the cells studied.
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