Metabolism Characteristics of Th17 and Regulatory T Cells in Autoimmune Diseases.

Yan Qin,Chong Gao,Jing Luo

doi:10.3389/fimmu.2022.828191

Abstract

The abnormal number and functional deficiency of immune cells are the pathological basis of various diseases. Recent years, the imbalance of Th17/regulatory T (Treg) cell underlies the occurrence and development of inflammation in autoimmune diseases (AID). Currently, studies have shown that material and energy metabolism is essential for maintaining cell survival and normal functions and the altered metabolic state of immune cells exists in a variety of AID. This review summarizes the biology and functions of Th17 and Treg cells in AID, with emphasis on the advances of the roles and regulatory mechanisms of energy metabolism in activation, differentiation and physiological function of Th17 and Treg cells, which will facilitate to provide targets for the treatment of immune-mediated diseases.

Highlights

In T cell biology, immunometabolism is intrinsically linked to cellular development, activation, function, differentiation and survival [1, 2]
Naïve T cells are maintained in a state of hyporesponsiveness called quiescence, which is characterized by small cell size, low proliferative rate, and low basal metabolism
IL-1b is another important proinflammatory factor that induces T help 17 subset (Th17) cell differentiation, mainly through activation of the mammalian targets for rapamycin (mTOR) pathway [21, 22]. mTOR activates catabolic pathways, especially aerobic glycolysis, and induces fatty acid synthesis (FAS), promoting T cell receptor (TCR)-mediated naive T cells to differentiate into Th17 cells [23]

Summary

Introduction

In T cell biology, immunometabolism is intrinsically linked to cellular development, activation, function, differentiation and survival [1, 2]. Th17 and Treg Cell Metabolism oxidation (FAO) to glycolysis, glutamine hydrolysis, and pentose phosphate pathways (PPP), thereby promoting T cell differentiation and proliferation [8, 12]. MTOR activates catabolic pathways, especially aerobic glycolysis, and induces fatty acid synthesis (FAS), promoting TCR-mediated naive T cells to differentiate into Th17 cells [23].

Results

Conclusion