Acquired immunity to Leishmaniasis is cell mediated (CMI) (4.5). Two subpopulation of CD4+T cells determine the outcome of disease by Leishmania infection. Cure in genetically resistant mice and immunity in vaccinated susceptible BALB/c H-2K mice correlates with the presence of a high frequency of Thy2+ CD4+T cell subsets (6.9). These observations raise the following questions: (i) What T cell epitopes are involved in the activation of protective versus disease promoting TH subsets?, and, (ii) What are the properties of the different T cell epitopes?, and, (iii) How do these epitopes influence the interaction of the MHC (Ia) molecule with the TCRa/B in order to selectively activate a TH subset? The above questions are amenable to investigation using Leishmania antigens. This is because, there are candidate Leishmania strain and stage specific antigens that either induce protective immunity or exacerbate disease by selectively activating a specific subset of primed TH cells (7,10,14). Therefore, we propose that the expression of the antigens is regulated in a stage and strain specific manner. The identification of these antigens and their genes from stage and strain specific cDNA library is possible. Sequence information and T cell proliferative assay would lead to the identification of the T cell epitopes. The presence of a relevant animal model, with a wealth of immunological information will facilitate the establishment of the relationship between antigen structure and function in vivo.
