Key result
Regulatory T cells show atheroprotective effects experimentally, but their clinical role remains unproven.
Why the study?
The roles of regulatory T cells in atherosclerosis in the clinical setting remain to be further characterized despite established importance in experimental studies.
Regulatory T cells exhibit atheroprotective mechanisms in experimental models, highlighting a potential therapeutic target for atherosclerosis that requires further clinical validation.
Atherosclerosis is a chronic autoimmune inflammatory disease. The involvement of both innate and adaptive immune responses in the pathogenesis of the disease has been well recognized. Tregs are an essential part of the immune system and have indispensable functions in maintaining immune system homeostasis, mediating peripheral tolerance, preventing autoimmune diseases, and suppressing inflammatory and proatherogenic immune response. Tregs carry out their immunosuppressive functions via several mechansims. One of the well-documented suppressive mechanisms of Tregs is the secretion of anti-inflammatory cytokines including IL-10, TGF-β, and IL-35. Studies have found that IL-10 and TGF-β have atheroprotective properties. In addition, Tregs can suppress the activity of proatherogenic effector T cells, suggesting an atheroprotective role. In fact, fewer Tregs are found in atherogenic ApoE−/− mice comparing to wild-type mice, suggesting an uncontrolled balance between weakened Tregs and effector T cells in atherogenesis. Some clinical studies of autoimmune diseases also suggest that decreased Tregs numbers are associated with increased disease activity. The importance of Tregs in many autoimmune diseases and experimental atherosclerosis has been established in in vivo and in vitro studies. However, the roles of Tregs in atherosclerosis in the clinical setting remains to be further characterized.
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Jahaira Lopez Pastrana (2013) conducted a review in Atherosclerosis. Regulatory T Cells (Tregs) was evaluated. Regulatory T cells demonstrate atheroprotective properties in experimental models via immunosuppressive mechanisms, but their specific role in clinical atherosclerosis remains to be characterized.
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