The effector function of platelets is induced and regulated by T lymphocytes.

The demonstration of effector functions of platelets in parasitic diseases raised the question of their possible regulation by T lymphocytes. Normal human platelets, treated with culture supernatants from antigen- or mitogen-stimulated CD4+/CD8- T cells, developed the capacity to kill young larvae of Schistosoma mansoni, in the absence of antibodies. The presence of IFN gamma in the lymphocyte supernatants, the neutralization by monoclonal anti-IFN gamma antibody, and the direct inducer effect of recombinant IFN gamma, clearly identify this lymphokine as one of the stimulator factors. In contrast, ConA- and antigen-stimulated human CD8+/CD4- T-cell supernatants contained a factor able to inhibit the IgE-dependent platelet cytotoxicity toward the same targets. The production of oxygen metabolites by IgE-coated platelets stimulated by anti-IgE was also strongly inhibited by this lymphokine. This platelet activity suppressive lymphokine (PASL) was identified as a polypeptide of 15 to 20 Kd with a pI of 4.6. The in vivo relevance of PASL was demonstrated by the complete abolition, after PASL treatment, of the protection normally conferred following a challenge infection by intravenous passive transfer of platelets from immune to normal rats.