title: Regulation of immunity during visceral Leishmania infection.
abstract: 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.
authors.affiliation: CNRS FR3636, Université Paris-Descartes, Paris, France. vasco.rodrigues@parisdescartes.fr.
authors.forename: Vasco
authors.initials: V
authors.lastname: Rodrigues
authors.affiliation: Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal. cordeiro@ibmc.up.pt.|Departamento de Ciências Biológicas, Faculdade de Farmácia, Universidade do Porto, Porto, Portugal. cordeiro@ibmc.up.pt.
authors.forename: Anabela
authors.initials: A
authors.lastname: Cordeiro-da-Silva
authors.affiliation: CNRS FR3636, Université Paris-Descartes, Paris, France. mirhaddad@gmail.com.
authors.forename: Mireille
authors.initials: M
authors.lastname: Laforge
authors.affiliation: School of Health Sciences, Life and Health Sciences Research Institute (ICVS), University of Minho, Braga, Portugal. ricardosilvestre@ecsaude.uminho.pt.|ICVS/3B's-PT Government Associate Laboratory, Braga, Guimarães, Portugal. ricardosilvestre@ecsaude.uminho.pt.
authors.forename: Ricardo
authors.initials: R
authors.lastname: Silvestre
authors.affiliation: CNRS FR3636, Université Paris-Descartes, Paris, France. estaquier@yahoo.fr.|Centre de Recherche en Infectiologie, Université Laval, Québec, Canada. estaquier@yahoo.fr.
authors.forename: Jérôme
authors.initials: J
authors.lastname: Estaquier
mesh_terms: D056704:Adaptive Immunity; D000818:Animals; D054884:Host-Pathogen Interactions; D006801:Humans; D007111:Immunity, Cellular; D056724:Immunity, Humoral; D007113:Immunity, Innate; D007891:Leishmania / Q000276:immunology* / Q000502:physiology*; D007898:Leishmaniasis, Visceral / Q000276:immunology* / Q000469:parasitology / Q000473:pathology*; D008099:Liver / Q000276:immunology / Q000469:parasitology / Q000473:pathology; D013154:Spleen / Q000276:immunology / Q000469:parasitology / Q000473:pathology