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Regulatory T cells in retroviral infections

Tight regulation of immune responses is not only critical for preventing autoimmune diseases but also for preventing immunopathological damage during infections in which overactive immune responses may be more harmful for the host than the pathogen itself. Regulatory T cells (Tregs) play a critical...

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Autores principales: Hasenkrug, Kim J., Chougnet, Claire A., Dittmer, Ulf
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5814043/
https://www.ncbi.nlm.nih.gov/pubmed/29447279
http://dx.doi.org/10.1371/journal.ppat.1006776
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author Hasenkrug, Kim J.
Chougnet, Claire A.
Dittmer, Ulf
author_facet Hasenkrug, Kim J.
Chougnet, Claire A.
Dittmer, Ulf
author_sort Hasenkrug, Kim J.
collection PubMed
description Tight regulation of immune responses is not only critical for preventing autoimmune diseases but also for preventing immunopathological damage during infections in which overactive immune responses may be more harmful for the host than the pathogen itself. Regulatory T cells (Tregs) play a critical role in this regulation, which was discovered using the Friend retrovirus (FV) mouse model. Subsequent FV studies revealed basic biological information about Tregs, including their suppressive activity on effector cells as well as the molecular mechanisms of virus-induced Treg expansion. Treg suppression not only limits immunopathology but also prevents complete elimination of pathogens contributing to chronic infections. Therefore, Tregs play a complex role in the pathogenesis of persistent retroviral infections. New therapeutic concepts to reactivate effector T-cell responses in chronic viral infections by manipulating Tregs also came from work with the FV model. This knowledge initiated many studies to characterize the role of Tregs in HIV pathogenesis in humans, where a complex picture is emerging. On one hand, Tregs suppress HIV-specific effector T-cell responses and are themselves targets of infection, but on the other hand, Tregs suppress HIV-induced immune hyperactivation and thus slow the infection of conventional CD4(+) T cells and limit immunopathology. In this review, the basic findings from the FV mouse model are put into perspective with clinical and basic research from HIV studies. In addition, the few Treg studies performed in the simian immunodeficiency virus (SIV) monkey model will also be discussed. The review provides a comprehensive picture of the diverse role of Tregs in different retroviral infections and possible therapeutic approaches to treat retroviral chronicity and pathogenesis by manipulating Treg responses.
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spelling pubmed-58140432018-03-02 Regulatory T cells in retroviral infections Hasenkrug, Kim J. Chougnet, Claire A. Dittmer, Ulf PLoS Pathog Review Tight regulation of immune responses is not only critical for preventing autoimmune diseases but also for preventing immunopathological damage during infections in which overactive immune responses may be more harmful for the host than the pathogen itself. Regulatory T cells (Tregs) play a critical role in this regulation, which was discovered using the Friend retrovirus (FV) mouse model. Subsequent FV studies revealed basic biological information about Tregs, including their suppressive activity on effector cells as well as the molecular mechanisms of virus-induced Treg expansion. Treg suppression not only limits immunopathology but also prevents complete elimination of pathogens contributing to chronic infections. Therefore, Tregs play a complex role in the pathogenesis of persistent retroviral infections. New therapeutic concepts to reactivate effector T-cell responses in chronic viral infections by manipulating Tregs also came from work with the FV model. This knowledge initiated many studies to characterize the role of Tregs in HIV pathogenesis in humans, where a complex picture is emerging. On one hand, Tregs suppress HIV-specific effector T-cell responses and are themselves targets of infection, but on the other hand, Tregs suppress HIV-induced immune hyperactivation and thus slow the infection of conventional CD4(+) T cells and limit immunopathology. In this review, the basic findings from the FV mouse model are put into perspective with clinical and basic research from HIV studies. In addition, the few Treg studies performed in the simian immunodeficiency virus (SIV) monkey model will also be discussed. The review provides a comprehensive picture of the diverse role of Tregs in different retroviral infections and possible therapeutic approaches to treat retroviral chronicity and pathogenesis by manipulating Treg responses. Public Library of Science 2018-02-15 /pmc/articles/PMC5814043/ /pubmed/29447279 http://dx.doi.org/10.1371/journal.ppat.1006776 Text en https://creativecommons.org/publicdomain/zero/1.0/ This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 (https://creativecommons.org/publicdomain/zero/1.0/) public domain dedication.
spellingShingle Review
Hasenkrug, Kim J.
Chougnet, Claire A.
Dittmer, Ulf
Regulatory T cells in retroviral infections
title Regulatory T cells in retroviral infections
title_full Regulatory T cells in retroviral infections
title_fullStr Regulatory T cells in retroviral infections
title_full_unstemmed Regulatory T cells in retroviral infections
title_short Regulatory T cells in retroviral infections
title_sort regulatory t cells in retroviral infections
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5814043/
https://www.ncbi.nlm.nih.gov/pubmed/29447279
http://dx.doi.org/10.1371/journal.ppat.1006776
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