Journal
CURRENT RHEUMATOLOGY REPORTS
Volume 18, Issue 12, Pages -Publisher
SPRINGER
DOI: 10.1007/s11926-016-0622-8
Keywords
Mitochondria; Mechanistic target of rapamycin; Systemic lupus erythematosus; Anti-phospholipid antibodies; T cells; B cells; Macrophages; Liver; Kidney
Categories
Funding
- National Institutes of Health [AI072648, DK078922, AI122176, AI048079, AR068052]
- Pfizer [P0468X1-4470/WS1234172]
- American College of Rheumatology Research Foundation
- Central New York Community Foundation
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The mechanistic target of rapamycin (mTOR) is a central regulator in cell growth, activation, proliferation, and survival. Activation of the mTOR pathway underlies the pathogenesis of systemic lupus erythematosus (SLE). While mTOR activation and its therapeutic reversal were originally discovered in T cells, recent investigations have also uncovered roles in other cell subsets including B cells, macrophages, and non-immune organs such as the liver and the kidney. Activation of mTOR complex 1 (mTORC1) precedes the onset of SLE and associated co-morbidities, such as anti-phospholipid syndrome (APS), and may act as an early marker of disease pathogenesis. Six case reports have now been published that document the development of SLE in patients with genetic activation of mTORC1. Targeting mTORC1 over-activation with N-acetylcysteine, rapamycin, and rapalogs provides an opportunity to supplant current therapies with severe side effect profiles such as prednisone or cyclophosphamide. In the present review, we will discuss the recent explosion of findings in support for a central role for mTOR activation in SLE.
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