Evaluation of Leishmania Homologue of Activated C Kinase (LACK) of Leishmania donovani in comparison to glycoprotein 63 as vaccine candidate against visceral leishmaniasis
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Leishmaniasis, caused by Leishmania protozoa transmitted via sand fly bites, affects over 12 million people annually, manifesting as self-limiting cutaneous lesions or fatal visceral leishmaniasis (VL). The disease immune response involves a Th1/Th2 paradigm, with Th1 promoting resistance and Th2 linked to susceptibility. Despite no available human vaccine, the Leishmania homologue of activated C kinase (LACK) protein has shown promise as a candidate due to its conservation across species. In this study, we purified native 34-kDa LACK protein from Leishmania donovani promastigotes and compared its efficacy with gp63 in cationic DSPC liposomes. While gp63 exhibited protective efficacy, LACK failed to protect BALB/c mice. Recombinant LACK, which was cloned, expressed, and purified, also did not confer protection. Immunological assays revealed a Th2-biased immune response characterised by a high IgG1/IgG2a ratio, elevated Th2 cytokines, and an unaltered delayed-type hypersensitivity (DTH) response, highlighting its limited potential.
