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The The clinical spectrum of leprosy reflects the striking differences between individuals in developing cell-mediated immunity to the causative agent, Mycobacterium leprae (7,8). At the "high resistant" pole of this spectrum, tuberculoid leprosy (TT) patients develop strong cellular immune responses to M. leprae antigens and efficiently eliminate the bacilli, whereas at the "low resistant" pole, lepromatous leprosy (LL) patients fail to mount specific T-cell responses to M. leprae antigens and develop a multibacillary disseminated disease (9). Several lines of evidence suggest that the M. leprae-specific T-cell nonresponsiveness observed in LL patients is not due to an absence ofM. leprae-reactive T cells or to defective antigen presentation as claimed in earlier reports (10, 11) but may be due to active down-regulation of M. leprae-specific T-cell responses, presumably by suppressor T (Ts) cells induced by M. leprae (12-14). Supporting this latter premise, we and others have previously isolated CD4+ and CD8+ T-cell clones from the peripheral blood and skin lesions of LL patients and shown that these T cells specifically suppress mycobacterium-specific T-cell responses in vitro (15-17). Previous analyses of these Ts clones revealed that they, like M. leprae-induced Th cells, express T-cell receptor (TCR) a and , ( chains and are restricted by HLA-DR or HLA-DQ molecules (15,16,18,38

These results confirm that platelets indeed express HLA-C. Furthermore, the results support the insignificant role of HLA-C in immunological platelet refractoriness.