Immunosuppression in leprosy
Sasiain, M.C.; de la Barrera, S.
Medicina 49(3): 213-215
1989
ISSN/ISBN: 0025-7680 PMID: 2535042 Document Number: 345802
Many authors tried to show that in lepromatous leprosy (LL), suppressor mechanisms are involved in the immune response. We have previously shown that non-specific suppression (Con A induced) was impaired in LL patients and tends to normalize during the erythema nodosum leprosum episode (ENL). In this system we have shown that CD8+ cells (Leu 2a+) can interfere with the generation of Con A-induced suppression. We also observed that a high percentage of LL patients had an increased spontaneous suppression. In these patients, the number of Leu 2a+ cells added in the assay did not correlate with the suppression values. On the other hand, we had demonstrated that the monocyte suppressor system may have an important role, due to the release of soluble factors (PGE2). We evaluated Mycobacterium leprae-induced suppressor cell function using a two step assay, on T cell proliferation. The results of this study indicate that the ability of M. leprae to induce suppressor activity was lower in LL patients than in tuberculoid (TT), intermediate clinical forms (BB, BL, BT) and BCG-immunized controls. On the other hand, we determined that the proportion of peripheral blood mononuclear cells (PBMC) bearing the Leu 8+ antigen (associated to suppressor inducer cells) was low in LL and tends to normalize during the ENL episode. Suppression of proliferation could not be overcome with exogenous IL-2 and was not related to the induction of Tac antigen. The ability of LL, TT, ENL and normal cells to proliferate upon PHA or Con A stimulus was similar. These results indicate that the defect in the generation of in vitro suppression by M. leprae in LL occurred during the induction period and could be associated with the reduction of Leu 8+ cells. We believe that the low frequency of Leu 8 positive cells in LL is a clue to the inability of LL-PBMC to generate specific and non-specific suppression of T cell proliferation.