Immune Response to Leishmaniasis

Leishmaniasis is a disease of zoonotic importance caused by intracellular group of protozoan parasites of genus Leishmania, which is biologically transmitted by sand fly (Phlebotomus spp.). The cutaneous form of disease is predominant in north-western region while visceral form is predominant in eastern region of India. The parasite escapes from humoral immune response by hiding as an amastigote in the lysosomes of the host macrophage. Being a parasite, Leishmania ensure its own survival by modulating host immune system by abnormal activation of protein kinase C, inhibition of MHC-protein production, induction of PGE2 and down regulation of TNF-α and membrane attack complex. The resistance is mediated by activation of T-helper 1 (Th1) cells which secretes Interleukin-2 (IL-2) and Interferon-□ (IFN-□). IFN-□ activates macrophages to express iNOS2, the enzyme catalysing the formation of nitric oxide. Nitric oxide kills the intracellular amastigotes. In contrast T-helper-2 immune response limits the action of Th1 functions via IL10 and IL-4, which deactivates macrophages helping intracellular parasite growth and disease progression