Setting the stage for Leishmania

Abstract

When a host is infected with a parasite, a symbiosis ensues that functions as a new complex organism; the infected host. The co-existence of these organisms requires integration of both physiological complexes. It has been shown that the immune system plays an important role in the fate of Leishmania in the host. White blood cells produce a cytokine context that either allows survival of the parasite or its elimination. This is dependent on the type of T-cell response activated upon infection. A T-helper 1 (Th1) response (characterized by the production of IFN-γ and IL-12) that leads to parasite killing owing to the activation of infected macrophages by IFN-γ. By contrast, a Th2 response (characterized by the production of IL- 4) allows survival of the parasite, probably because of downregulation of IFN-γ production by IL-10. Results from a mouse model indicated that salivary gland lysates of Plebotomus papatasi, the mosquito vector that transmits Leishmania major, provokes a Th2 response, which allows parasite survival (M.L. Mbow. et al., J. Immunol. 161, 5571–5577, 1998). Recently, it was shown that prior exposure of mice to bites of uninfected sandflies induced strong Th1 responsiveness with IFN-γ production, and associated resistance to Leishmania infection. These results suggest an alternative means of immunization against Leishmania infection (S. Kamhawi et al., Science 290, 1351–1354, 2000) and might have implications to the epidemiology of the disease. TS