Recent developments in systemic lupus erythematosus pathogenesis and applications for therapy

Recent developments in systemic lupus erythematosus pathogenesis and applications for therapy Purpose of reviewSystemic lupus erythematosus (SLE) pathogenesis is complex. Aberrancies of immune function that previously were described but not well understood are now becoming better characterized, in part through recognition of monogenic cases of lupus-like disease.Recent findingsWe highlight here recent descriptions of metabolic dysfunction, cytokine dysregulation, signaling defects, and DNA damage pathways in SLE. Specifically, we review the effects of signaling abnormalities in mammalian target of rapamycin, Rho kinase, Bruton's tyrosine kinase, and Ras pathways. The importance of DNA damage sensing and repair pathways, and their influence on the overproduction of type I interferon in SLE are also reviewed.SummaryRecent findings in SLE pathogenesis expand on previous understandings of broad immune dysfunction. These findings have clinical applications, as the dysregulated pathways described here can be targeted by existing and preclinical therapies. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Current Opinion in Rheumatology Wolters Kluwer Health

Recent developments in systemic lupus erythematosus pathogenesis and applications for therapy

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Publisher
Wolters Kluwer Health
Copyright
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
ISSN
1040-8711
eISSN
1531-6963
D.O.I.
10.1097/BOR.0000000000000474
Publisher site
See Article on Publisher Site

Abstract

Purpose of reviewSystemic lupus erythematosus (SLE) pathogenesis is complex. Aberrancies of immune function that previously were described but not well understood are now becoming better characterized, in part through recognition of monogenic cases of lupus-like disease.Recent findingsWe highlight here recent descriptions of metabolic dysfunction, cytokine dysregulation, signaling defects, and DNA damage pathways in SLE. Specifically, we review the effects of signaling abnormalities in mammalian target of rapamycin, Rho kinase, Bruton's tyrosine kinase, and Ras pathways. The importance of DNA damage sensing and repair pathways, and their influence on the overproduction of type I interferon in SLE are also reviewed.SummaryRecent findings in SLE pathogenesis expand on previous understandings of broad immune dysfunction. These findings have clinical applications, as the dysregulated pathways described here can be targeted by existing and preclinical therapies.

Journal

Current Opinion in RheumatologyWolters Kluwer Health

Published: Mar 1, 2018

References

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