Notably, the vaccinated hamsters’elicited strongest DTH reaction among other experimental groups suggesting a Monoammoniumglycyrrhizinate correlation between CMI responses and Labetalol hydrochloride immunity to infection. Herein too, a significant DTH response was observed in the hamsters vaccinated with rLdEno+BCG and rLdAld+BCG. It is well established that the cytokine milieu at the initiation of infection is critical in determining disease outcome. So to understand the interplay between the disease healing inflammatory cytokines IFN-c and IL-12 and disease associated cytokines IL-10 and IL-4, the expression of these cytokines as well as the level of iNOS transcript was investigated by qRT-PCR. As the reagents for cytokine estimation in hamsters is commercially unavailable, herein quantitative real time PCR was used for assessing the expression of cytokine mRNAs in the experimental groups. The immune response generated thereof in vaccinated hamsters was clearly associated with a Th1-type cytokine response predominantly, as indicated by the upregulation of iNOS, IFN-c, and IL-12, along with simultaneous downregulation of TGF-b, IL4, and IL-10. Transcripts of IFN-c and TNF-a, often reported to act in concert to activate iNOS for the production of NO, showed manifold increase in all the immunized groups of hamsters. It is also suggested that TNF-a is one of the primary agents to stimulate macrophage to produce NO. Our results are in consistence with the studies of Bhowmick et al in which the control of disease progression and parasite burden in vaccinated mice was associated with augmentation of antigenspecific IFN-c production and down-regulation of IL-4, demonstrating a Th1 bias. High levels of IL-4 and IL-10 that has been observed in unimmunized infected control animals supported the view that marked up-regulation of these two cytokines is accompanied by susceptibility, disease progression and depressed Th1 type of cell mediated immunity. The presence of IL-4, IL-10 and TGF-b in infected hamsters are reported to be the major immunosuppressive cytokines in experimental and human VL. The studies of Lehmann et al also established that in VL a Th1 dominated immune response is protective and, furthermore, the capacity to produce IFN- c rather than the presence of IL-4 determines the efficacy of the immune response in susceptible mice. In addition, a marked decrease in the expression of IL-10 in vaccinated hamsters, which was not observed in positive control, may be due to an inhibitory effect of IFN-c in the expression of this cytokine. TGF-b,a pleiotropic cytokine with diverse functions, is known to be expressed at a moderate level even in normal hamsters. TGF-b is also known to inhibit the activities of immune cells and was found to be down-regulated in vaccinated hamsters compared with the infected controls. Unlike the findings of, where they could not detect IL- 4 transcripts at all in splenocytes of.90% of the infected hamsters, it was quite evident in this study. Further, there was apparent down regulation of IL-4 expression in all the immunized hamsters throughout the experiment. Moreover, active VL is also associated with the production of high levels of the Leishmania specific antibody which is observed before detection of parasite-specific T cell response. The progressive elevation of the anti-Leishmania IgG and IgG1 in all the experimental groups except the vaccinated groups, compared with the level of IgG2, which was significantly and consistently prominent in the vaccinated groups, suggested that protection against leishmaniasis is induced by a strong T cell response. These observations further support the views that protection against leishmaniasis is induced by a strong T-cell response and almost undetectable amounts of antibodies.