Autophagy and immune response in kidneys.
Autophagy is a ubiquitous intracellular catabolic process that contributes to homeostatic maintenance and regulates the balance between health and disease. Emerging evidence from both the immunology and renal literature suggests that important relationships exist between the immune system and renal autophagy that may have significant implications for our understanding of the pathogenesis of kidney diseases. Autophagic flux in renal parenchymal cells can protect against acute and chronic kidney injury and can be stimulated via activation of innate immune receptors, cytokine secretion, and/or direct contact by immune cells. Conversely, modulation of autophagy in renal cells may influence both adaptive and innate immune cell responses. Autophagy can promote the ability of renal epithelial cells, which can act as antigen-presenting cells, to process and present self-antigen to immune cells. In addition, autophagic control of inflammasome function can modify the intrarenal inflammatory milieu, thereby preventing immune cell infiltration. Because autophagy and immune responses may promote or protect against kidney injury, further research is needed to better understand how interactions between renal parenchymal cells and the immune system are altered by autophagy. Novel agents are being developed that promote or inhibit various steps of the autophagy pathway, and it is likely that whether such agents are beneficial or harmful in the context of kidney disease will depend, at least in part, on whether and how they influence the relationship between autophagy and the immune response in the kidney.
Renal Division, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY; Renal Division, James J Peters Bronx VA Hospital, Bronx, NY. Electronic address: jeremy.leventhal@mssm.ed.
Jeremy S
JS
Leventhal
Renal Division, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY; Renal Division, James J Peters Bronx VA Hospital, Bronx, NY.
John C
JC
He
Renal Division, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY.
Michael J
MJ
Ross
D058186:Acute Kidney Injury / Q000473:pathology; D000818:Animals; D017951:Antigen Presentation; D001343:Autophagy / Q000502:physiology*; D016207:Cytokines / Q000502:physiology; D000949:Histocompatibility Antigens Class II / Q000276:immunology; D006801:Humans; D058847:Inflammasomes / Q000502:physiology; D007668:Kidney / Q000276:immunology*; D051436:Renal Insufficiency, Chronic / Q000473:pathology
D016207:Cytokines; D000949:Histocompatibility Antigens Class II; D058847:Inflammasomes
Autophagy; acute kidney injury; cytokine; inflammasome; innate immunity; kidney