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

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 immuno-suppressive, 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 system-atically summarize the role of the mTOR signaling pathway in SLE pathogenesis, Treg cell dysfunction and SLE treatment.

Automated summary

This review systematically summarizes the role of the mTOR signaling pathway in the pathogenesis of systemic lupus erythematosus (SLE), regulatory T cell dysfunction, and the treatment of SLE.