The major histocompatibility complex (MHC) controls of the outcome of the immune response to T cell‐dependent antigens by dictating whether T cell responsiveness will result (MHC‐immune response [Ir] genes) or alternatively T cell nonresponsiveness will occur, possibly through the activation of suppressor cells (MHC‐immune suppression [Is] genes). In mice, I‐A molecules typically restrict antigen‐specific helper T cells. In contrast, H‐2 I‐E molecules have been reported to control nonresponsiveness to a variety of antigens through antigen‐specific suppressor cells. In analogy, HLA‐DR molecules are the dominant restriction elements for helper Tcells in man. This forces the question whether DQ molecules may be involved in controlling nonresponsiveness in man, e.g. through suppression. In one system, T cell nonresponsiveness to Schistosoma japonicum, evidence has been presented supporting this notion. We have now used a second system, Mycobacterium leprae‐specific T cell nonresponsiveness, that is typically found in lepromatous leprosy patients. We find positive but limited evidence for a role for HLA‐DQ molecules in controlling Tcell nonresponsiveness to M. leprae of the 22 nonresponder patients tested, 4 showed a proliferative T cell response to M. leprae after the addition of DQ‐ but not DR‐specific mAb to the cell cultures. In one of the four BCG nonresponders, anti‐DQ mAb had a similar effect.
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