Abstract
Human leishmaniasis constitutes a diverse group of diseases caused by protozoa of the genus Leishmania. The parasites are transmitted by sandflies and the infection is initiated by introduction of promastigotes into the skin at the site of the vector’s bite. In the mammalian host, Leishmania parasites exist as obligatory intracellular amastigotes residing in mononuclear phagocytes. The diseases vary in severity from the self-healing cutaneous leishmaniasis, characterized by a localized cutaneous lesion at the site of primary infection, to the progressive visceral leishmaniasis, where the parasites disseminate from the original skin lesion to local lymph nodes and then to spleen, liver and bone marrow. The clinical manifestation depends primarily on the species of parasite, but also on the genetic make-up of the host. The T cell-mediated immunity is crucial for the outcome of infection because activated T cells release various lymphokines that promote either the spreading or the elimination of parasites1,2.
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© 1993 Plenum Press, New York
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Moll, H. (1993). Experimental Cutaneous Leishmaniasis: Langerhans Cells Internalize Leishmania Major and Induce an Antigen-Specific T-Cell Response. In: Kamperdijk, E.W.A., Nieuwenhuis, P., Hoefsmit, E.C.M. (eds) Dendritic Cells in Fundamental and Clinical Immunology. Advances in Experimental Medicine and Biology, vol 329. Springer, New York, NY. https://doi.org/10.1007/978-1-4615-2930-9_98
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DOI: https://doi.org/10.1007/978-1-4615-2930-9_98
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