Subversion of Immunity by Leishmania amazonensis Parasites: Possible Role of Phosphatidylserine as a Main Regulator

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...

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Main Authors: Joao Luiz Mendes Wanderley, Jaqueline França Costa, Valéria Matos Borges, Marcello Barcinski
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:Journal of Parasitology Research
Online Access:http://dx.doi.org/10.1155/2012/981686
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author Joao Luiz Mendes Wanderley
Jaqueline França Costa
Valéria Matos Borges
Marcello Barcinski
author_facet Joao Luiz Mendes Wanderley
Jaqueline França Costa
Valéria Matos Borges
Marcello Barcinski
author_sort Joao Luiz Mendes Wanderley
collection DOAJ
description 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.
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institution Kabale University
issn 2090-0023
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language English
publishDate 2012-01-01
publisher Wiley
record_format Article
series Journal of Parasitology Research
spelling doaj-art-34b2c748e311407ba87b987f51541c2c2025-02-03T01:01:52ZengWileyJournal of Parasitology Research2090-00232090-00312012-01-01201210.1155/2012/981686981686Subversion of Immunity by Leishmania amazonensis Parasites: Possible Role of Phosphatidylserine as a Main RegulatorJoao Luiz Mendes Wanderley0Jaqueline França Costa1Valéria Matos Borges2Marcello Barcinski3Universidade Federal do Rio de Janeiro, Pólo Universitário Macaé, BrazilCentro de Pesquisa Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador, BA, BrazilCentro de Pesquisa Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador, BA, BrazilLaboratório de Biologia Celular, Instituto Oswaldo Cruz, Rio de Janeiro, RJ, BrazilLeishmania 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.http://dx.doi.org/10.1155/2012/981686
spellingShingle Joao Luiz Mendes Wanderley
Jaqueline França Costa
Valéria Matos Borges
Marcello Barcinski
Subversion of Immunity by Leishmania amazonensis Parasites: Possible Role of Phosphatidylserine as a Main Regulator
Journal of Parasitology Research
title Subversion of Immunity by Leishmania amazonensis Parasites: Possible Role of Phosphatidylserine as a Main Regulator
title_full Subversion of Immunity by Leishmania amazonensis Parasites: Possible Role of Phosphatidylserine as a Main Regulator
title_fullStr Subversion of Immunity by Leishmania amazonensis Parasites: Possible Role of Phosphatidylserine as a Main Regulator
title_full_unstemmed Subversion of Immunity by Leishmania amazonensis Parasites: Possible Role of Phosphatidylserine as a Main Regulator
title_short Subversion of Immunity by Leishmania amazonensis Parasites: Possible Role of Phosphatidylserine as a Main Regulator
title_sort subversion of immunity by leishmania amazonensis parasites possible role of phosphatidylserine as a main regulator
url http://dx.doi.org/10.1155/2012/981686
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