SUMMARYExposure of Brown Norway rats to mercuric chloride induces systemic autoimmunity, involving T-and B-lymphocyte activation, (auto-)antibody production and multiorgan in¯ammation. Several divalent metal ions, such as Mg 2+ and Mn 2+ , can activate binding of integrins to their ligands, thus causing lymphocyte adhesion. To test the hypothesis that Hg 2+ acts in a similar way, we studied the effect of HgCl 2 on integrin-mediated T-cell adhesion. HgCl 2 induced cell±cell aggregation of human T lymphoblasts. Exposure of a human T-cell clone to HgCl 2 for 1 hr enhanced, in a dose-dependent way, cell binding to ®bronectin (FN) and to intercellular adhesion molecules (ICAM) -1, -2 and -3. Furthermore, HgCl 2 induced strong binding of Jurkat T cells to FN. These effects of HgCl 2 were of similar magnitude as the effects of phorbol 12-myristate 13-acetate (PMA) or MnCl 2 . Studies using blocking antibodies indicated the involvement of CD11a in binding to ICAMs, and of CD49d, CD49e, and CD29 in binding to FN. Adhesion to FN induced by HgCl 2 or by PMA, but not by MnCl 2 , was dependent on temperature and on extracellular Ca 2+ or Mg 2+ . Addition of cytochalasin B enhanced synergistically the FN adhesion induced by MnCl 2 , whereas the effects of PMA and HgCl 2 were not modi®ed. These results indicate that Hg 2+ is a potent activator of T-cell adhesion, mediated by several integrins and ligands. In contrast to the effect of MnCl 2 , HgCl 2 -induced cell adhesion probably involves an intracellular pathway. Activation of integrins by HgCl 2 may play an important role in activation and migration of leucocytes involved in HgCl 2 -induced immune dysregulation in vivo.

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