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Cells 2019, 8(2), 138; https://doi.org/10.3390/cells8020138

Modulation of Autophagy for Controlling Immunity

1
Research Group of Natural Materials and Metabolism, Korea Food Research Institute, Wanjugun 55365, Korea
2
Department of Agricultural Biotechnology, Seoul National University, Seoul 08826, Korea
3
Division of Bioengineering, Incheon National University, Incheon 22012, Korea
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Received: 31 December 2018 / Revised: 1 February 2019 / Accepted: 7 February 2019 / Published: 9 February 2019
(This article belongs to the Special Issue Autophagy in Age-Related Human Diseases)
Full-Text   |   PDF [791 KB, uploaded 19 February 2019]   |  

Abstract

Autophagy is an essential process that maintains physiological homeostasis by promoting the transfer of cytoplasmic constituents to autophagolysosomes for degradation. In immune cells, the autophagy pathway plays an additional role in facilitating proper immunological functions. Specifically, the autophagy pathway can participate in controlling key steps in innate and adaptive immunity. Accordingly, alterations in autophagy have been linked to inflammatory diseases and defective immune responses against pathogens. In this review, we discuss the various roles of autophagy signaling in coordinating immune responses and how these activities are connected to pathological conditions. We highlight the therapeutic potential of autophagy modulators that can impact immune responses and the mechanisms of action responsible. View Full-Text
Keywords: autophagy; innate immunity; adaptive immunity; modulators autophagy; innate immunity; adaptive immunity; modulators
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Jang, Y.J.; Kim, J.H.; Byun, S. Modulation of Autophagy for Controlling Immunity. Cells 2019, 8, 138.

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