Abstract
CD4+ T cells play a vital role in the adaptive immune system and are involved in the pathogenesis of many diseases, including cancer, autoimmune diseases, and chronic inflammation. As an important mechanism for energy storage, a lot of researches have clarified that metabolism imbalance interacts with immune disorder, and one leads to the other. Lipid metabolism has close relationship with CD4+ T cells. In this review, we discuss fatty acid, cholesterol, prostaglandin, and phospholipid metabolism in CD4+ T cell subsets. Fatty acid β-oxidation (FAO) is activated in Th17 cell to support the proinflammatory function. Cholesterol promotes Th1, Th2, and Treg cell differentiation. In addition to glucose metabolism, lipid metabolism is also very important for immunity. Here, it is highlighted that lipid metabolism regulates CD4+ T cell differentiation and function and is related to diseases.
Highlights
Different CD4+ T cell subsets are involved in various immune responses
It has been established that lipid metabolism is of vital importance in CD4+ T cell activation and differentiation (Figure 1)
The activation of mevalonate pathway is essential for Treg cell differentiation, while hardly any information is known about de novo cholesterol biosynthesis in Th1 or Th17 cells
Summary
Different CD4+ T cell subsets are involved in various immune responses. Th1 cells are responsible for an increased cellmediated immune response, especially cellular functions against pathogen infections. Raptor/mTORC1 signaling in Treg cells promotes cholesterol biosynthesis, which is essential for Treg cell suppressive activity [1]. We focus on how fatty acids, cholesterol, prostaglandins, and phospholipids metabolisms are involved in CD4+ T cell function. Effector T cell differentiation depends on de novo fatty acid synthesis, and it is heatedly discussed whether FAO is required for Treg cell differentiation [10,11,12].
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