Expression of receptors for sheep red blood cells and the ability to proliferate in response to phytohaemagglutinin (PHA) are the traditional properties of human T cells1,2, but the function of the sheep red cell receptor (the T11 antigen) is controversial3,4 and the mechanism of PHA-induced mitogenesis unclear. Mitogenesis involves a complex series of cell-mediated and factor-dependent interactions, but a rise in intracellular free calcium concentration, [Ca2+]i, seems to be an important primary event in T-cell activation5-7. We have now investigated the effects of three monoclonal antibodies, previously shown to inhibit mitogen-induced proliferation3,8,9, on T-cell [Ca 2+]i. We find that anti-LFA-2 and OKT11, which react with the sheep red cell receptor8,10, have no effect on [Ca 2+]i, nor do they inhibit the rise in [Ca 2+]i induced by concanavalin A (Con A) or the mitogenic anti-T3 monoclonal antibody UCHT1 (ref. 11). They do, however, block PHA-induced Ca2+ mobilization. Anti-LFA-1, which reacts with the lymphocyte function-associated antigen8,12, has no effect on intracellular Ca2+. These studies suggest that the sheep red blood cell receptor is an activation pathway for T cells and that the effects of PHA are mediated through this pathway.
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