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Interactions between Autophagy and Inhibitory Cytokines

Autophagy is a degradative pathway that plays an essential role in maintaining cellular homeostasis. Most early studies of autophagy focused on its involvement in age-associated degeneration and nutrient deprivation. However, the immunological functions of autophagy have become more widely studied i...

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Detalles Bibliográficos
Autores principales: Wu, Tian-tian, Li, Wei-Min, Yao, Yong-Ming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4910606/
https://www.ncbi.nlm.nih.gov/pubmed/27313501
http://dx.doi.org/10.7150/ijbs.15194
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author Wu, Tian-tian
Li, Wei-Min
Yao, Yong-Ming
author_facet Wu, Tian-tian
Li, Wei-Min
Yao, Yong-Ming
author_sort Wu, Tian-tian
collection PubMed
description Autophagy is a degradative pathway that plays an essential role in maintaining cellular homeostasis. Most early studies of autophagy focused on its involvement in age-associated degeneration and nutrient deprivation. However, the immunological functions of autophagy have become more widely studied in recent years. Autophagy has been shown to be an intrinsic cellular defense mechanism in the innate and adaptive immune responses. Cytokines belong to a broad and loose category of proteins and are crucial for innate and adaptive immunity. Inhibitory cytokines have evolved to permit tolerance to self while also contributing to the eradication of invading pathogens. Interactions between inhibitory cytokines and autophagy have recently been reported, revealing a novel mechanism by which autophagy controls the immune response. In this review, we discuss interactions between autophagy and the regulatory cytokines IL-10, transforming growth factor-β, and IL-27. We also mention possible interactions between two newly discovered cytokines, IL-35 and IL-37, and autophagy.
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spelling pubmed-49106062016-06-16 Interactions between Autophagy and Inhibitory Cytokines Wu, Tian-tian Li, Wei-Min Yao, Yong-Ming Int J Biol Sci Review Autophagy is a degradative pathway that plays an essential role in maintaining cellular homeostasis. Most early studies of autophagy focused on its involvement in age-associated degeneration and nutrient deprivation. However, the immunological functions of autophagy have become more widely studied in recent years. Autophagy has been shown to be an intrinsic cellular defense mechanism in the innate and adaptive immune responses. Cytokines belong to a broad and loose category of proteins and are crucial for innate and adaptive immunity. Inhibitory cytokines have evolved to permit tolerance to self while also contributing to the eradication of invading pathogens. Interactions between inhibitory cytokines and autophagy have recently been reported, revealing a novel mechanism by which autophagy controls the immune response. In this review, we discuss interactions between autophagy and the regulatory cytokines IL-10, transforming growth factor-β, and IL-27. We also mention possible interactions between two newly discovered cytokines, IL-35 and IL-37, and autophagy. Ivyspring International Publisher 2016-06-07 /pmc/articles/PMC4910606/ /pubmed/27313501 http://dx.doi.org/10.7150/ijbs.15194 Text en © Ivyspring International Publisher. Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited. See http://ivyspring.com/terms for terms and conditions.
spellingShingle Review
Wu, Tian-tian
Li, Wei-Min
Yao, Yong-Ming
Interactions between Autophagy and Inhibitory Cytokines
title Interactions between Autophagy and Inhibitory Cytokines
title_full Interactions between Autophagy and Inhibitory Cytokines
title_fullStr Interactions between Autophagy and Inhibitory Cytokines
title_full_unstemmed Interactions between Autophagy and Inhibitory Cytokines
title_short Interactions between Autophagy and Inhibitory Cytokines
title_sort interactions between autophagy and inhibitory cytokines
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4910606/
https://www.ncbi.nlm.nih.gov/pubmed/27313501
http://dx.doi.org/10.7150/ijbs.15194
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