Role of Interleukin-10 in Malaria: Focusing on Coinfection with Lethal and Nonlethal Murine Malaria Parasites

Interleukin- (IL-) 10, anti-inflammatory cytokine, is known to inhibit the protective immune responses against malaria parasites and to be involved in exacerbating parasitemia during Plasmodium infection. In contrast, IL-10 is regarded as necessary for suppressing severe pathology during Plasmodium...

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Main Authors: Mamoru Niikura, Shin-Ichi Inoue, Fumie Kobayashi
Format: Article
Language:English
Published: Hindawi Limited 2011-01-01
Series:Journal of Biomedicine and Biotechnology
Online Access:http://dx.doi.org/10.1155/2011/383962
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spelling doaj-db7c98295f9c4e6bb073f58bc3032b9d2020-11-24T21:47:11ZengHindawi LimitedJournal of Biomedicine and Biotechnology1110-72431110-72512011-01-01201110.1155/2011/383962383962Role of Interleukin-10 in Malaria: Focusing on Coinfection with Lethal and Nonlethal Murine Malaria ParasitesMamoru Niikura0Shin-Ichi Inoue1Fumie Kobayashi2Department of Infectious Diseases, Kyorin University School of Medicine, Tokyo 181-8611, JapanDepartment of Infectious Diseases, Kyorin University School of Medicine, Tokyo 181-8611, JapanDepartment of Infectious Diseases, Kyorin University School of Medicine, Tokyo 181-8611, JapanInterleukin- (IL-) 10, anti-inflammatory cytokine, is known to inhibit the protective immune responses against malaria parasites and to be involved in exacerbating parasitemia during Plasmodium infection. In contrast, IL-10 is regarded as necessary for suppressing severe pathology during Plasmodium infection. Here, we summarize the role of IL-10 during murine malaria infection, focusing especially on coinfection with lethal and nonlethal strains of malaria parasites. Recent studies have demonstrated that the major sources of IL-10 are subpopulations of CD4+ T cells in humans and mice infected with Plasmodium. We also discuss the influence of innate immunity on the induction of CD4+ T cells during murine malaria coinfection.http://dx.doi.org/10.1155/2011/383962
collection DOAJ
language English
format Article
sources DOAJ
author Mamoru Niikura
Shin-Ichi Inoue
Fumie Kobayashi
spellingShingle Mamoru Niikura
Shin-Ichi Inoue
Fumie Kobayashi
Role of Interleukin-10 in Malaria: Focusing on Coinfection with Lethal and Nonlethal Murine Malaria Parasites
Journal of Biomedicine and Biotechnology
author_facet Mamoru Niikura
Shin-Ichi Inoue
Fumie Kobayashi
author_sort Mamoru Niikura
title Role of Interleukin-10 in Malaria: Focusing on Coinfection with Lethal and Nonlethal Murine Malaria Parasites
title_short Role of Interleukin-10 in Malaria: Focusing on Coinfection with Lethal and Nonlethal Murine Malaria Parasites
title_full Role of Interleukin-10 in Malaria: Focusing on Coinfection with Lethal and Nonlethal Murine Malaria Parasites
title_fullStr Role of Interleukin-10 in Malaria: Focusing on Coinfection with Lethal and Nonlethal Murine Malaria Parasites
title_full_unstemmed Role of Interleukin-10 in Malaria: Focusing on Coinfection with Lethal and Nonlethal Murine Malaria Parasites
title_sort role of interleukin-10 in malaria: focusing on coinfection with lethal and nonlethal murine malaria parasites
publisher Hindawi Limited
series Journal of Biomedicine and Biotechnology
issn 1110-7243
1110-7251
publishDate 2011-01-01
description Interleukin- (IL-) 10, anti-inflammatory cytokine, is known to inhibit the protective immune responses against malaria parasites and to be involved in exacerbating parasitemia during Plasmodium infection. In contrast, IL-10 is regarded as necessary for suppressing severe pathology during Plasmodium infection. Here, we summarize the role of IL-10 during murine malaria infection, focusing especially on coinfection with lethal and nonlethal strains of malaria parasites. Recent studies have demonstrated that the major sources of IL-10 are subpopulations of CD4+ T cells in humans and mice infected with Plasmodium. We also discuss the influence of innate immunity on the induction of CD4+ T cells during murine malaria coinfection.
url http://dx.doi.org/10.1155/2011/383962
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