mTOR signaling: A pivotal player in Treg cell dysfunction in systemic lupus erythematosus.

Abstract

Systemic lupus erythematosus (SLE) is a typical autoimmune disease characterized by multiorgan involvement and marked variability in clinical presentation. SLE pathogenesis includes regulatory T cell dysfunction and antinuclear antibody production. Mammalian target of rapamycin (mTOR), a serine/threonine kinase in the phosphoinositide 3-kinase (PI3K)-related kinase family, is a therapeutic target for autoimmune diseases such as SLE. Rapamycin, an inhibitor of the mTOR signaling pathway, is a macrolide antibiotic with potent immunosuppressive, antiproliferative and antifibrotic effects. Recently, an increasing number of studies have investigated the role of mTOR in regulatory T (Treg) cells and its impact on SLE pathogenesis. This review aims to systematically summarize the role of the mTOR signaling pathway in SLE pathogenesis, Treg cell dysfunction and SLE treatment.

• Authors: Xingyun Zhao, Shifen Wang, Shengjun Wang, Jue Xie, Dawei Cui
• Journal: Clinical immunology (Orlando, Fla.) (Clin Immunol) Vol. 245 Pg. 109153 (12 2022) ISSN: 1521-7035 [Electronic] United States
• PMID: 36265758 (Publication Type: Journal Article, Review, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2022 Elsevier Inc. All rights reserved.

Chemical References

• Phosphatidylinositol 3-Kinases
• TOR Serine-Threonine Kinases
• Sirolimus
• MTOR protein, human

Topics

• Humans
• T-Lymphocytes, Regulatory (metabolism)
• Phosphatidylinositol 3-Kinases (metabolism)
• TOR Serine-Threonine Kinases (metabolism)
• Lupus Erythematosus, Systemic
• Signal Transduction
• Sirolimus (pharmacology)
• Autoimmune Diseases (drug therapy)