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Type I Interferons and Malaria: A Double-Edge Sword Against a Complex Parasitic Disease

Type I interferons (IFN-Is) are important cytokines playing critical roles in various infections, autoimmune diseases, and cancer. Studies have also shown that IFN-Is exhibit ‘conflicting’ roles in malaria parasite infections. Malaria parasites have a complex life cycle with multiple developing stag...

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Autores principales: He, Xiao, Xia, Lu, Tumas, Keyla C., Wu, Jian, Su, Xin-Zhuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7738626/
https://www.ncbi.nlm.nih.gov/pubmed/33344264
http://dx.doi.org/10.3389/fcimb.2020.594621
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author He, Xiao
Xia, Lu
Tumas, Keyla C.
Wu, Jian
Su, Xin-Zhuan
author_facet He, Xiao
Xia, Lu
Tumas, Keyla C.
Wu, Jian
Su, Xin-Zhuan
author_sort He, Xiao
collection PubMed
description Type I interferons (IFN-Is) are important cytokines playing critical roles in various infections, autoimmune diseases, and cancer. Studies have also shown that IFN-Is exhibit ‘conflicting’ roles in malaria parasite infections. Malaria parasites have a complex life cycle with multiple developing stages in two hosts. Both the liver and blood stages of malaria parasites in a vertebrate host stimulate IFN-I responses. IFN-Is have been shown to inhibit liver and blood stage development, to suppress T cell activation and adaptive immune response, and to promote production of proinflammatory cytokines and chemokines in animal models. Different parasite species or strains trigger distinct IFN-I responses. For example, a Plasmodium yoelii strain can stimulate a strong IFN-I response during early infection, whereas its isogenetic strain does not. Host genetic background also greatly influences IFN-I production during malaria infections. Consequently, the effects of IFN-Is on parasitemia and disease symptoms are highly variable depending on the combination of parasite and host species or strains. Toll-like receptor (TLR) 7, TLR9, melanoma differentiation-associated protein 5 (MDA5), and cyclic GMP-AMP synthase (cGAS) coupled with stimulator of interferon genes (STING) are the major receptors for recognizing parasite nucleic acids (RNA/DNA) to trigger IFN-I responses. IFN-I levels in vivo are tightly regulated, and various novel molecules have been identified to regulate IFN-I responses during malaria infections. Here we review the major findings and progress in ligand recognition, signaling pathways, functions, and regulation of IFN-I responses during malaria infections.
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spelling pubmed-77386262020-12-17 Type I Interferons and Malaria: A Double-Edge Sword Against a Complex Parasitic Disease He, Xiao Xia, Lu Tumas, Keyla C. Wu, Jian Su, Xin-Zhuan Front Cell Infect Microbiol Cellular and Infection Microbiology Type I interferons (IFN-Is) are important cytokines playing critical roles in various infections, autoimmune diseases, and cancer. Studies have also shown that IFN-Is exhibit ‘conflicting’ roles in malaria parasite infections. Malaria parasites have a complex life cycle with multiple developing stages in two hosts. Both the liver and blood stages of malaria parasites in a vertebrate host stimulate IFN-I responses. IFN-Is have been shown to inhibit liver and blood stage development, to suppress T cell activation and adaptive immune response, and to promote production of proinflammatory cytokines and chemokines in animal models. Different parasite species or strains trigger distinct IFN-I responses. For example, a Plasmodium yoelii strain can stimulate a strong IFN-I response during early infection, whereas its isogenetic strain does not. Host genetic background also greatly influences IFN-I production during malaria infections. Consequently, the effects of IFN-Is on parasitemia and disease symptoms are highly variable depending on the combination of parasite and host species or strains. Toll-like receptor (TLR) 7, TLR9, melanoma differentiation-associated protein 5 (MDA5), and cyclic GMP-AMP synthase (cGAS) coupled with stimulator of interferon genes (STING) are the major receptors for recognizing parasite nucleic acids (RNA/DNA) to trigger IFN-I responses. IFN-I levels in vivo are tightly regulated, and various novel molecules have been identified to regulate IFN-I responses during malaria infections. Here we review the major findings and progress in ligand recognition, signaling pathways, functions, and regulation of IFN-I responses during malaria infections. Frontiers Media S.A. 2020-12-02 /pmc/articles/PMC7738626/ /pubmed/33344264 http://dx.doi.org/10.3389/fcimb.2020.594621 Text en Copyright © 2020 He, Xia, Tumas, Wu and Su http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cellular and Infection Microbiology
He, Xiao
Xia, Lu
Tumas, Keyla C.
Wu, Jian
Su, Xin-Zhuan
Type I Interferons and Malaria: A Double-Edge Sword Against a Complex Parasitic Disease
title Type I Interferons and Malaria: A Double-Edge Sword Against a Complex Parasitic Disease
title_full Type I Interferons and Malaria: A Double-Edge Sword Against a Complex Parasitic Disease
title_fullStr Type I Interferons and Malaria: A Double-Edge Sword Against a Complex Parasitic Disease
title_full_unstemmed Type I Interferons and Malaria: A Double-Edge Sword Against a Complex Parasitic Disease
title_short Type I Interferons and Malaria: A Double-Edge Sword Against a Complex Parasitic Disease
title_sort type i interferons and malaria: a double-edge sword against a complex parasitic disease
topic Cellular and Infection Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7738626/
https://www.ncbi.nlm.nih.gov/pubmed/33344264
http://dx.doi.org/10.3389/fcimb.2020.594621
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