Immunobiology of leishmaniasis.

Leishmaniasis is a parasitic disease caused by various species of Leishmania, a unicellular kinetoplastid protozoan flagellate. It manifests mainly in 3 clinical forms; visceral leishmaniasis (VL), cutaneous leishmaniasis (CL) and mucocutaneous leishmaniasis (MCL), of which VL is the most severe form of the disease. VL is lethal if untreated and spontaneous cure is extremely rare. Cutaneous leishmaniasis usually has milder course and often results into a self-healing of ulcers. Resolution of leishmanial infection is dependent on the coordinated interactions between components of cell mediated immune response, specifically the activation of targeted T-cell populations for appropriate cytokine production and activation of macrophages. In murine model, the development of Thl response is associated with control of infection, and Th2 response is associated with disease progression. However, Th1 and Th2 dichotomy in the human system is not as distinct as in mice and the murine model does not strictly apply to human leishmaniasis. This review focuses the dichotomy of immune response against various clinical forms of the disease. An in-depth knowledge of sequences involved in the immune response to the parasite would help in designing prophylactic and therapeutic strategies against leishmaniasis.