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      Autophagy and inflammation

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          Abstract

          Autophagy is a homeostatic mechanism involved in the disposal of damaged organelles, denatured proteins as well as invaded pathogens through a lysosomal degradation pathway. Recently, increasing evidences have demonstrated its role in both innate and adaptive immunity, and thereby influence the pathogenesis of inflammatory diseases. The detection of autophagy machinery facilitated the measurement of autophagy during physiological and pathophysiological processes. Autophagy plays critical roles in inflammation through influencing the development, homeostasis and survival of inflammatory cells, including macrophages, neutrophils and lymphocytes; effecting the transcription, processing and secretion of a number of cytokines, as well as being regulated by cytokines. Recently, autophagy-dependent mechanisms have been studied in the pathogenesis of several inflammatory diseases, including infectious diseases, Crohn’s disease, cystic fibrosis, pulmonary hypertension, chronic obstructive pulmonary diseases and so on. These studies suggested that modulation of autophagy might lead to therapeutic interventions for diseases associated with inflammation. Here we highlight recent advances in investigating the roles of autophagy in inflammation as well as inflammatory diseases.

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          Most cited references105

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          Autophagosome formation: core machinery and adaptations.

          Eukaryotic cells employ autophagy to degrade damaged or obsolete organelles and proteins. Central to this process is the formation of autophagosomes, double-membrane vesicles responsible for delivering cytoplasmic material to lysosomes. In the past decade many autophagy-related genes, ATG, have been identified that are required for selective and/or nonselective autophagic functions. In all types of autophagy, a core molecular machinery has a critical role in forming sequestering vesicles, the autophagosome, which is the hallmark morphological feature of this dynamic process. Additional components allow autophagy to adapt to the changing needs of the cell.
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            Autophagy-dependent viral recognition by plasmacytoid dendritic cells.

            Plasmacytoid dendritic cells (pDCs) detect viruses in the acidified endosomes by means of Toll-like receptors (TLRs). Yet, pDC responses to certain single-stranded RNA (ssRNA) viruses occur only after live viral infection. We present evidence here that the recognition of such viruses by TLR7 requires transport of cytosolic viral replication intermediates into the lysosome by the process of autophagy. In addition, autophagy was found to be required for the production of interferon-alpha by pDCs. These results support a key role for autophagy in mediating ssRNA virus detection and interferon-alpha secretion by pDCs and suggest that cytosolic replication intermediates of viruses serve as pathogen signatures recognized by TLR7.
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              Isolation and characterization of autophagy-defective mutants ofSaccharomyces cerevisiae

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                Author and article information

                Contributors
                shilver-s-dream@hotmail.com
                fangxiaocong@gmail.com
                xiangdong.wang@clintransmed.org
                Journal
                Clin Transl Med
                Clin Transl Med
                Clinical and Translational Medicine
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                2001-1326
                26 July 2017
                26 July 2017
                2017
                : 6
                : 24
                Affiliations
                ISNI 0000 0001 0125 2443, GRID grid.8547.e, Zhongshan Hospital Institute of Clinical Science, Shanghai Institute of Clinical Bioinformatics, , Fudan University Medical School, ; Shanghai, China
                Article
                154
                10.1186/s40169-017-0154-5
                5529308
                28748360
                8b99f4d6-a4be-427d-9903-74e117fed11d
                © The Author(s) 2017

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 21 March 2017
                : 18 July 2017
                Categories
                Review
                Custom metadata
                © The Author(s) 2017

                Medicine
                autophagy,inflammation,inflammatory diseases
                Medicine
                autophagy, inflammation, inflammatory diseases

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