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Regulation of immunity during visceral Leishmania infection
- Rodrigues, Vasco, Cordeiro-da-Silva, Anabela, Laforge, Mireille, Silvestre, Ricardo, Estaquier, Jérôme
- Parasites & vectors 2016 v.9 no.1 pp. 118
- Leishmania, T-lymphocytes, amastigotes, cytokines, drug therapy, eukaryotic cells, humoral immunity, immune response, immunotherapy, leishmaniasis, liver, phagocytes, spleen, vaccines
- Unicellular eukaryotes of the genus Leishmania are collectively responsible for a heterogeneous group of diseases known as leishmaniasis. The visceral form of leishmaniasis, caused by L. donovani or L. infantum, is a devastating condition, claiming 20,000 to 40,000 lives annually, with particular incidence in some of the poorest regions of the world. Immunity to Leishmania depends on the development of protective type I immune responses capable of activating infected phagocytes to kill intracellular amastigotes. However, despite the induction of protective responses, disease progresses due to a multitude of factors that impede an optimal response. These include the action of suppressive cytokines, exhaustion of specific T cells, loss of lymphoid tissue architecture and a defective humoral response. We will review how these responses are orchestrated during the course of infection, including both early and chronic stages, focusing on the spleen and the liver, which are the main target organs of visceral Leishmania in the host. A comprehensive understanding of the immune events that occur during visceral Leishmania infection is crucial for the implementation of immunotherapeutic approaches that complement the current anti-Leishmania chemotherapy and the development of effective vaccines to prevent disease.