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Therapeutic adoptive transfer of natural regulatory T cells (nTreg, CD4 +  CD25 +  Foxp3 +  T cells) or in vivo selective expansion of nTreg cells has been demonstrated to improve the cardiac function in various cardiovascular disease models. The differentiation of nTreg cells is mediated by catecholamines via β 1 -adrenergic receptor (β 1 -AR) activation. Autoantibody against β 1 -adrenoceptor (β 1 -AA) as a β 1 -AR agonist is closely associated with the occurrence and deterioration of cardiac dysfunction. However, whether β 1 -AA has any impact on nTreg cells has not been reported. The aim of the present study was intended to assess the potential impact of β 1 -AA on nTreg cell differentiation and explore the underlying mechanism. It was found that the expression of multiple proteins involved in nTreg cell differentiation, immunosuppressive function, and migration was up-regulated in mice after β 1 -AA administration, suggesting that β 1 -AA may promote nTreg cell activation. In vitro, β 1 -AA promoted nTreg cell differentiation by up-regulating mitochondrial fatty acid oxidation (FAO) in activated CD4 +  T cells via AMP-activated protein kinase (AMPK) activation and mitochondrial membrane potential reduction. In addition, the AMPK agonist facilitated β 1 -AA-mediated FAO and nTreg cell differentiation. To further confirm the role of AMPK in β 1 -AA-mediated nTreg cell differentiation, β 1 -AA was acted on the CD4 +  T cells isolated from AMPK-deficient (AMPK −/− ) mice. The result showed that the effect of β 1 -AA on nTreg cell differentiation was attenuated markedly after AMPK knockout. In conclusion, AMPK-mediated metabolic regulation targeting for nTreg cell restoration may be a promising therapeutic target for β 1 -AA-positive patients with cardiac dysfunction.

cell death and disease

Autoantibody against β1-adrenoceptor promotes the differentiation of natural regulatory T cells from activated CD4+ T cells by up-regulating AMPK-mediated fatty acid oxidation