Autophagy in autoimmune disease

Verfasser / Beitragende:
[Zhen Yang, Jörg Goronzy, Cornelia Weyand]
Ort, Verlag, Jahr:
2015
Enthalten in:
Journal of Molecular Medicine, 93/7(2015-07-01), 707-717
Format:
Artikel (online)
ID: 605543143
LEADER caa a22 4500
001 605543143
003 CHVBK
005 20210128100925.0
007 cr unu---uuuuu
008 210128e20150701xx s 000 0 eng
024 7 0 |a 10.1007/s00109-015-1297-8  |2 doi 
035 |a (NATIONALLICENCE)springer-10.1007/s00109-015-1297-8 
245 0 0 |a Autophagy in autoimmune disease  |h [Elektronische Daten]  |c [Zhen Yang, Jörg Goronzy, Cornelia Weyand] 
520 3 |a Autophagy is a protective and life-sustaining process in which cytoplasmic components are packaged into double-membrane vesicles and targeted to lysosomes for degradation. This process of cellular self-digestion is an essential stress response and is cytoprotective by removing damaged organelles and proteins that threaten the cell's survival. Key outcomes include energy generation and recycling of metabolic precursors. In the immune system, autophagy regulates processes such as antigen uptake and presentation, removal of pathogens, survival of short- and long-lived immune cells, and cytokine-dependent inflammation. In all cases, a window of optimal autophagic activity appears critical to balance catabolic, reparative, and inflammation-inducing processes. Dysregulation of autophagosome formation and autophagic flux can have deleterious consequences, ranging from a failure to "clean house” to the induction of autophagy-induced cell death. Abnormalities in the autophagic pathway have been implicated in numerous autoimmune diseases. Genome-wide association studies have linked polymorphisms in autophagy-related genes with predisposition for tissue-destructive inflammatory disease, specifically in inflammatory bowel disease and systemic lupus erythematosus. Although the precise mechanisms by which dysfunctional autophagy renders the host susceptible to continuous inflammation remain unclear, autophagy's role in regulating the long-term survival of adaptive immune cells has recently surfaced as a defect in multiple sclerosis and rheumatoid arthritis. Efforts are underway to identify autophagy-inducing and autophagy-suppressing pharmacologic interventions that can be added to immunosuppressive therapy to improve outcomes of patients with autoimmune disease. 
540 |a Springer-Verlag Berlin Heidelberg, 2015 
690 7 |a Autophagy  |2 nationallicence 
690 7 |a Autoimmune disease  |2 nationallicence 
690 7 |a Rheumatoid arthritis  |2 nationallicence 
690 7 |a Systemic lupus erythematosus  |2 nationallicence 
690 7 |a Crohn's disease  |2 nationallicence 
690 7 |a Multiple sclerosis  |2 nationallicence 
700 1 |a Yang  |D Zhen  |u Department of Medicine, Stanford University School of Medicine, CCSR Building Rm 2225, 269 Campus Drive West, 94305-5166, Stanford, CA, USA  |4 aut 
700 1 |a Goronzy  |D Jörg  |u Department of Medicine, Stanford University School of Medicine, CCSR Building Rm 2225, 269 Campus Drive West, 94305-5166, Stanford, CA, USA  |4 aut 
700 1 |a Weyand  |D Cornelia  |u Department of Medicine, Stanford University School of Medicine, CCSR Building Rm 2225, 269 Campus Drive West, 94305-5166, Stanford, CA, USA  |4 aut 
773 0 |t Journal of Molecular Medicine  |d Springer Berlin Heidelberg  |g 93/7(2015-07-01), 707-717  |x 0946-2716  |q 93:7<707  |1 2015  |2 93  |o 109 
856 4 0 |u https://doi.org/10.1007/s00109-015-1297-8  |q text/html  |z Onlinezugriff via DOI 
898 |a BK010053  |b XK010053  |c XK010000 
900 7 |a Metadata rights reserved  |b Springer special CC-BY-NC licence  |2 nationallicence 
908 |D 1  |a review-article  |2 jats 
949 |B NATIONALLICENCE  |F NATIONALLICENCE  |b NL-springer 
950 |B NATIONALLICENCE  |P 856  |E 40  |u https://doi.org/10.1007/s00109-015-1297-8  |q text/html  |z Onlinezugriff via DOI 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Yang  |D Zhen  |u Department of Medicine, Stanford University School of Medicine, CCSR Building Rm 2225, 269 Campus Drive West, 94305-5166, Stanford, CA, USA  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Goronzy  |D Jörg  |u Department of Medicine, Stanford University School of Medicine, CCSR Building Rm 2225, 269 Campus Drive West, 94305-5166, Stanford, CA, USA  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Weyand  |D Cornelia  |u Department of Medicine, Stanford University School of Medicine, CCSR Building Rm 2225, 269 Campus Drive West, 94305-5166, Stanford, CA, USA  |4 aut 
950 |B NATIONALLICENCE  |P 773  |E 0-  |t Journal of Molecular Medicine  |d Springer Berlin Heidelberg  |g 93/7(2015-07-01), 707-717  |x 0946-2716  |q 93:7<707  |1 2015  |2 93  |o 109