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Autophagy and immunological aberrations in systemic lupus erythematosus
Systemic lupus erythematosus (SLE) is a complex autoimmune disease, in which immune defects can occur at multiple points of the cascading auto‐aggressive immune reactions, resulting in a striking heterogeneity of clinical presentations. The clinical manifestations of such autoimmune response can be...
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Published in: | European journal of immunology 2019-04, Vol.49 (4), p.523-533 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Systemic lupus erythematosus (SLE) is a complex autoimmune disease, in which immune defects can occur at multiple points of the cascading auto‐aggressive immune reactions, resulting in a striking heterogeneity of clinical presentations. The clinical manifestations of such autoimmune response can be severe: common manifestations symptoms include rash and renal inflammation progressing to kidney failure. Autophagy, the cellular “self‐digestion” process, is a key factor in the interplay between innate and adaptive immunity. Dysregulation of autophagy has been implicated in numerous autoimmune diseases. Several lines of evidence from genomic studies, cell culture systems, animal models, and human patients are emerging to support the role of autophagy in progression and pathogenesis of SLE. In this review, we summarize recent key findings on the aberrations of autophagy in SLE, with a special focus on how deregulated autophagy promotes autoimmunity and renal damage. We will also discuss how the observed findings may be translated into therapeutic settings.
Genetic and environmental factors can promote the pathogenesis and/or development of SLE. Normal levels of autophagy contribute to the maintenance of the immune homeostasis, whereas up‐ or downregulated autophagy contributes to the loss of tolerance leading to autoantibodies production. We here review how immune cell autophagy is deregulated in lupus. |
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ISSN: | 0014-2980 1521-4141 |
DOI: | 10.1002/eji.201847679 |