Genetic control of the clinical manifestation of leprosy was investigated in 66 unrelated patients with leprosy and 8 multiplex families. In 32 lepromatous leprosy (LL) patients, both phenotype frequency of HLA-DR2 and haplotype frequency of HLA-B35-DR2-DQw1 were significantly increased. Our family data combined with other investigators' data showed that the distribution of shared HLA haplotypes differed significantly from the random distribution, thereby suggesting the existence of an HLA-linked major gene for lepromatous leprosy. To investigate the function of this major gene, the cellular mechanism of nonresponsiveness of LL that is strictly specific to Mycobacterium leprae (ML) antigen was analysed using panning technique and monoclonal antibodies. We have tested 30 LL patients for their suppressive activity of T8 cells on the T cell response to ML of tuberculoid leprosy (TT) patients. T8 cells from two LL patients abrogated the response of TT patients. None of LL patients tested showed proliferative response to ML antigen even when we removed the T8 cells from the culture. Therefore, we concluded that nonresponsiveness to ML antigen of LL patients in vitro was generated by the elimination of responding T cells. In the minor population of LL, T8 suppressor T cells were still active in peripheral blood. The T8 suppressor T cells might play some role in the elimination of responding T cells to ML antigen.
All Science Journal Classification (ASJC) codes
- Infectious Diseases