Abstract
Leishmania amazonensis parasites cause progressive disease in most inbred mouse strains and are associated with the development of diffuse cutaneous leishmaniasis in humans. The poor activation of an effective cellular response is correlated with the ability of these parasites to infect mononuclear phagocytic cells without triggering their activation or actively suppressing innate responses of these cells. Here we discuss the possible role of phosphatidylserine exposure by these parasites as a main regulator of the mechanism underlying subversion of the immune system at different steps during the infection.
Highlights
Leishmania amazonensis parasites cause progressive disease in most inbred mouse strains and are associated with the development of diffuse cutaneous leishmaniasis in humans
Diffuse cutaneous leishmaniasis (DCL) occurs when the parasite disseminates causing the appearance of multiple skin lesions, in distal sites relative to the transmission site [3]
BALB/c IL4 receptor knock-out (KO) mice remained susceptible to L. major infection when infected with LV39 strain, which seems to be due to an increased production of IL-10 by T cells [13]
Summary
Leishmania parasites are heteroxenous kinetoplastid protozoan organisms, which undergo complete differentiation upon a cycle of proliferation/differentiation in the midgut of phlebotomine sand flies followed by the transmission of infective metacyclic promastigotes [1, 2] to mammalian hosts during the insect blood meal. There are two main groups of parasites, stratified upon the clinical outcome of the infection: the ones capable of causing tegumentar and the ones capable of causing visceral diseases In both cases, disease is initiated by the bite of an infected sand fly, followed by the generation of a skin lesion, mainly caused by the inflammatory response induced on that site. Among the clinical manifestations observed in humans with the tegumentary disease, diffuse and mucocutaneous leishmaniasis are the most severe forms In both cases, most patients were found in the South and Central America, associated with L. amazonensis infection for DCL and L. braziliensis infection for MCL. Diffuse cutaneous leishmaniasis (DCL) is a rare clinical manifestation and is characterized by the appearance of several nonulcerated nodular skin lesions, uncontrolled parasite proliferation, an inefficient cellular immune response against parasite antigens, and resistance to most therapeutic strategies [5, 6]. The exhibition of markers of apoptosis by the parasite could be a contributing factor during host-parasite interactions as a possible immunosuppressive mechanism of DCL [7]
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