Unveiling the roles of autophagy in innate and adaptive immunity
Beth Levine,Vojo Deretic +1 more
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TLDR
The mechanisms of autophagy are described and recent advances relevant to the role of Autophagy in innate and adaptive immunity are highlighted.Abstract:
Cells digest portions of their interiors in a process known as autophagy to recycle nutrients, remodel and dispose of unwanted cytoplasmic constituents. This ancient pathway, conserved from yeast to humans, is now emerging as a central player in the immunological control of bacterial, parasitic and viral infections. The process of autophagy may degrade intracellular pathogens, deliver endogenous antigens to MHC-class-II-loading compartments, direct viral nucleic acids to Toll-like receptors and regulate T-cell homeostasis. This Review describes the mechanisms of autophagy and highlights recent advances relevant to the role of autophagy in innate and adaptive immunity.read more
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Journal ArticleDOI
Autophagy in the Pathogenesis of Disease
TL;DR: This Review summarizes recent advances in understanding the physiological functions of autophagy and its possible roles in the causation and prevention of human diseases.
Journal ArticleDOI
Autophagy fights disease through cellular self-digestion
TL;DR: Understanding autophagy may ultimately allow scientists and clinicians to harness this process for the purpose of improving human health, and to play a role in cell death.
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Repertoires of Autophagy in the Pathogenesis of Ocular Diseases
TL;DR: In this manuscript, the relevant progress about the role of autophagy in the pathogenesis of ocular diseases is reviewed and pharmacological manipulation of Autophagy may provide an alternative therapeutic target for some Ocular diseases.
Journal ArticleDOI
Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease
TL;DR: The endoplasmic reticulum is the major site in the cell for protein folding and trafficking and is central to many cellular functions and is emerging as a potential site for the intersection of inflammation and metabolic disease.
Journal ArticleDOI
The selective autophagy substrate p62 activates the stress responsive transcription factor Nrf2 through inactivation of Keap1
Masaaki Komatsu,Hirofumi Kurokawa,Satoshi Waguri,Keiko Taguchi,Akira Kobayashi,Yoshinobu Ichimura,Yoshinobu Ichimura,Yu-shin Sou,Yu-shin Sou,Izumi Ueno,Ayako Sakamoto,Kit I. Tong,Mihee Kim,Yasumasa Nishito,Shun-ichiro Iemura,Tohru Natsume,Takashi Ueno,Eiki Kominami,Hozumi Motohashi,Keiji Tanaka,Masayuki Yamamoto +20 more
TL;DR: The findings indicate that the pathological process associated with p62 accumulation results in hyperactivation of Nrf2 and delineates unexpected roles of selective autophagy in controlling the transcription of cellular defence enzyme genes.
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TL;DR: The physiological consequences of mammalianTORC1 dysregulation suggest that inhibitors of mammalian TOR may be useful in the treatment of cancer, cardiovascular disease, autoimmunity, and metabolic disorders.
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Development by Self-Digestion: Molecular Mechanisms and Biological Functions of Autophagy
Beth Levine,Daniel J. Klionsky +1 more
TL;DR: This review summarizes the current knowledge about the molecular machinery of autophagy and the role of the autophagic machinery in eukaryotic development and identifies a set of evolutionarily conserved genes that are essential forAutophagy.
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Autophagy as a Regulated Pathway of Cellular Degradation
Daniel J. Klionsky,Scott D. Emr +1 more
TL;DR: The core protein machinery that is necessary to drive formation and consumption of intermediates in the macroautophagy pathway includes a ubiquitin-like protein conjugation system and a protein complex that directs membrane docking and fusion at the lysosome or vacuole.
Journal ArticleDOI
Bcl-2 antiapoptotic proteins inhibit Beclin 1-dependent autophagy.
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TL;DR: Bcl-2 not only functions as an antiapoptotic protein, but also as an antiautophagy protein via its inhibitory interaction with Beclin 1, which may help maintain autophagy at levels that are compatible with cell survival, rather than cell death.