This observation was authenticated in endemic control and cured patients of VL wherein analogous results were observed, i.e. proliferation of lymphocytes in vitro and the release of very high amount of Th1type cytokines viz. IFN-c and IL-12p40 in response to rLdEno as well as rLdAld and compared with SLD. The induction of lymphocyte proliferation and IFN-c production by some of the recombinant antigens viz. gp63 in subjects cured of visceral form and in patients with cutaneous or mucosal leishmaniasis has been shown by different groups. These observations can be correlated with the well documented fact that IFN-c induces production of NO in phagocytic cells harbouring leishmania parasite, thereby killing them. The capacity to produce IFN-c after antigenic stimulation of immune lymphocytes may be an important indicator of effective cell-mediated immunity. Thus, the similar cellular responses to rLdEno as well as rLdAld in cured hamsters as well as in cured patients/endemic controls of VL indicate that the results so obtained with the hamster could be translated into humans. The limitations of this in vitro study based on a convenience human sampling, may not perhaps allow drawing solid conclusions regarding the immunogenicity of rLdEno as well as rLdAld. We further evaluated the prophylactic potential of rLdEno as well as rLdAld along with BCG in hamsters by challenging them with lethal dose of Leishmania. BCG had been used as an adjuvant with several immunizing agents since it has been reported that it Amikacin hydrate activates macrophages inducing NO and elicits long lasting cellular and humoral immune responses. Significant reduction in parasite load was noticed in rLdEno vaccinated hamsters and was supported by their longer survival period as compared to unvaccinated infected ones, while rLdAld provided only partial protection. A positive correlation of parasite loads with splenomegaly and hepatomegaly was observed among the experimental and control groups. Among the several parameters of CMI, one measure is Leishmania- specific LTT related to T cell stimulation with mitogens and antigen in vitro, which almost always accompanies control of parasite growth and healing in humans and animals. Since previous reports described that T cell proliferation is impaired during active VL, we explored rLdEno as well as rLdAld-induced T cell proliferation in hamsters vaccinated with rLdEno+BCG and rLdAld+BCG after L. donovani challenge at different time points of study. Significant LTT response in rLdEno+BCG vaccinated hamsters and,2 folds in rLdAld+BCG vaccinated hamsters was observed on days 45, 60 and 90 p.c. as compared to the other experimental as well as control groups. However, LTT itself is not the only primary effector mechanism of immunity, but rather the production of NO, upon stimulation of Leishmania-specific T cells, activates the macrophages to kill the intracellular parasites. In this study also, there was a gradual increase in NO production in the supernatant of macrophages co-stimulated with supernatant of rLdEno as well as rLdAld-stimulated lymphocytes from vaccinated hamsters which also support the view regarding the up-regulation of iNOS by Th1 cell associated cytokines. Successful vaccination of humans and animals is often related to antigen induced DTH responses in vivo which is characterized by activation and recruitment of predominantly T cells and macrophages at the site of intradermal injection in previously 4-(Benzyloxy)phenol sensitized host. DTH has been shown to be absolutely dependent on the presence of memory T-cells. Both the CD4+ and CD8+ fractions of cells have been shown to modulate an immune response. Contemporary debate regarding the reaction is focused on the role of the Th1 and Th2 cells.