Leishmaniasis: principles of the immune response and function of nitric oxide

Leishmania are flagellated protozoa, which are transmitted to mammals by sand flies. Depending on the parasite species and the host immune system, infection with Leishmania can lead to simple self-healing ulcers (e.g., oriental sore), progressive mucocutaneous lesions, or to visceral disease involving spleen, liver and bone marrow (kala azar). The control of the parasites is critically dependent on type 1 CD4+ T helper cells, which evolve in the presence of interleukin-12 and activate the macrophages for the killing of the intracellular, amastigote Leishmania stage through the production of interferon-gamma. The killing process involves reactive oxygen and nitrogen intermediates (e.g., NO). Anti-Leishmania antibodies are generated during the infection, but do not confer protection. In this article, the main components of immune response against Leishmania and the role of nitrogen monoxide (nitric oxide, NO) in the Leishmania major mouse model will be reviewed.