The Role of Autophagy in the Function of CD4+ T Cells and the Development of Chronic Inflammatory Diseases

被引:17
作者
Jeong, Jiung [1 ,2 ]
Choi, Young Joon [1 ]
Lee, Heung Kyu [1 ]
机构
[1] Korea Adv Inst Sci & Technol KAIST, Grad Sch Med Sci & Engn, Daejeon, South Korea
[2] Seoul Natl Univ Hosp, Dept Internal Med, Seoul, South Korea
基金
新加坡国家研究基金会;
关键词
autophagy; CD4+T cell; asthma; Crohn's disease; rheumatoid arthritis; multiple sclerosis; systemic lupus erythematosus; ANTIOXIDANT SYSTEM; KINASE VPS34; DIFFERENTIATION; DEGRADATION; CONTRIBUTES; HOMEOSTASIS; MECHANISMS; VARIANT; ATG5; MACROAUTOPHAGY;
D O I
10.3389/fphar.2022.860146
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Uncontrolled acute inflammation progresses to persistent inflammation that leads to various chronic inflammatory diseases, including asthma, Crohn's disease, rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus. CD4(+) T cells are key immune cells that determine the development of these chronic inflammatory diseases. CD4(+) T cells orchestrate adaptive immune responses by producing cytokines and effector molecules. These functional roles of T cells vary depending on the surrounding inflammatory or anatomical environment. Autophagy is an important process that can regulate the function of CD4(+) T cells. By lysosomal degradation of cytoplasmic materials, autophagy mediates CD4(+) T cell-mediated immune responses, including cytokine production, proliferation, and differentiation. Furthermore, through canonical processes involving autophagy machinery, autophagy also contributes to the development of chronic inflammatory diseases. Therefore, a targeted intervention of autophagy processes could be used to treat chronic inflammatory diseases. This review focuses on the role of autophagy via CD4(+) T cells in the pathogenesis and treatment of such diseases. In particular, we explore the underlying mechanisms of autophagy in the regulation of CD4(+) T cell metabolism, survival, development, proliferation, differentiation, and aging. Furthermore, we suggest that autophagy-mediated modulation of CD4(+) T cells is a promising therapeutic target for treating chronic inflammatory diseases.
引用
收藏
页数:15
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[21]   Estrogen and CD4+ T cells [J].
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[30]   Increased autophagy in CD4+ T cells of rheumatoid arthritis patients results in T-cell hyperactivation and apoptosis resistance [J].
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