The Role of the Immune System in Resistance to Infection

Leishmaniasis is a spectrum of diseases with clinical symptoms ranging in severity from skin lesions to serious disfigurement and fatal systemic infection. The outcome of infection depends on the parasite species as well as host genetic factors and immune competence. In order to develop a successful infection, the Leishmania must evade both the innate and adaptive immune responses. Whilst protective immunity has been driven by Th1-type T cell responses, the role of Th2-type cytokines is not entirely clear, although it has been implicated in susceptibility to leishmaniasis. A successful treatment of all the forms of leishmaniasis depends on efficient elimination of parasites by activated macrophages. Paradoxically, Leishmania species have evolved a variety of strategies to evade leishmanicidal mechanisms and survive in macrophages in the phagosome. Interestingly, most infected individuals develop long-lasting protective immunity following primary infection; however, sterile immunity is hardly ever achieved and parasites are believed to persist asymptomatically in the host. The vast array of immune cells and cytokines involved in the immune response to Leishmania clearly highlights the complexity of the disease and reveals a complicated net of regulatory and counter-regulatory interactions. This chapter outlines our current knowledge of the immune factors implicated in the disease and discusses the role the immune system plays in resistance to infection.