Most clinical cases of cutaneous leishmaniasis caused by Leishmania tropica major consist of self-healing lesions that are associated with the development of strong specific cell-mediated immunity (CMI) detected by delayed-type hypersensitivity (DTH). At the other extreme are susceptible individuals who develop persistent or diffuse forms of the disease. This spectrum of cutaneous leishmaniasis can be reproduced in in-bred mouse strains according to their genetic constitution. BALB/c mice are exceptionally susceptible: the disease can be induced with minimum infecting doses and is inexorably progressive, terminating in cutaneous and fatal visceral metastasis. In this case, potentially curative CMI is abrogated by the generation of a specific Lyt-1$2-, I-J- population of suppressor T (Ts) cells, whose induction is probably secondary to a primary macrophage defect controlled by a single major non-H-2-linked autosomal gene. The generation of the Ts cells can be prevented and infection cured by prior sublethal (550 rad) irradiation. The potency of the Ts cells is such that as few as 10(6) cells transferred adoptively can completely reverse this prophylactic effect. In view of their potency and potential relevance to clinical leishmaniasis, I have now studied Ts cells at the clonal level to delineate further their functional characteristics and interaction with the effector mechanism. I report here a cloned T-cell line expressing specific suppression against in vitro lymphocyte proliferation and in vitro induction of DTH to L. tropica antigens.