Control of CD4^(+) T cells to restrain inflammatory diseases via eukaryotic elongation factor 2 kinase
作者机构：Department of Microbial Pathogenesis and ImmunologyTexas A&M University Health Science CenterBryanTX77807USA Department of Biochemistry and BiophysicsTexas A&M UniversityCollege StationTX77843USA Department of Veterinary PathobiologyTexas A&M UniversityCollege StationTX77845USA Department of Toxicology and Cancer BiologyDepartment of Pharmacology and Nutritional Scienceand Markey Cancer CenterUniversity of Kentucky College of MedicineLexingtonKY40536USA
出 版 物：《Signal Transduction and Targeted Therapy》 (信号转导与靶向治疗（英文）)
年 卷 期：2023年第8卷第11期
页 面：5503-5517页
核心收录：
学科分类：1001[医学-基础医学(可授医学、理学学位)] 100102[医学-免疫学] 10[医学]
基 金：We thank Dr. Alexey Ryazonov (Rutgers University, Robert Wood Johnson Medical School, New Jersey) for the generous gifts of eEF2K KO mice. We thank Mr. Eber Villazana and Ms. Aspen Pham at Texas Aamp M University for blinded monitored arthritis and coliti
主 题：inflammatory diseases inflammation
摘 要：CD4^(+)T cells,particularly IL-17-secreting helper CD4^(+)T cells,play a central role in the inflammatory processes underlying autoimmune *** Elongation Factor 2 Kinase(eEF2K)is pivotal in CD8^(+)T cells and has important implications in vascular dysfunction and inflammation-related diseases such as ***,its specific immunological role in CD4^(+)T cell activities and related inflammatory diseases remains *** investigation has uncovered that the deficiency of eEF2K disrupts the survival and proliferation of CD4^(+)T cells,impairs their ability to secrete ***,this dysregulation leads to heightened production of pro-inflammatory cytokine IL-17,fosters a pro-inflammatory microenvironment in the absence of eEF2K in CD4^(+)T ***,the absence of eEF2K in CD4^(+)T cells is linked to increased metabolic activity and mitochondrial *** have shown that eEF2K regulates mitochondrial function and CD4^(+)T cell activity through the upregulation of the transcription factor,signal transducer and activator of transcription 3(STAT3).Crucially,the deficiency of eEF2K exacerbates the severity of inflammation-related diseases,including rheumatoid arthritis,multiple sclerosis,and ulcerative ***,the use of C188-9,a small molecule targeting STAT3,mitigates colitis in a murine immunodeficiency model receiving eEF2K knockout(KO)CD4^(+)T *** findings emphasize the pivotal role of eEF2K in controlling the function and metabolism of CD4^(+)T cells and its indispensable involvement in inflammation-related *** eEF2K represents a promising avenue for novel therapeutic approaches in the treatment of inflammation-related disorders.
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