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Remodeling of T-cell mitochondrial metabolism to treat autoimmune diseases.
Lin, Liyan; Ren, Ruyu; Xiong, Qiao; Zheng, Chunfu; Yang, Bin; Wang, Huiqing.
Afiliación
  • Lin L; Department of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu 610041, China; Sichuan Clinical Research Center for Laboratory Medicine, Chengdu 610041, China; Laboratory Medicine Research Center of West China Hospital, Sichuan University, Chengdu 610041, China.
  • Ren R; Department of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu 610041, China; Sichuan Clinical Research Center for Laboratory Medicine, Chengdu 610041, China; Laboratory Medicine Research Center of West China Hospital, Sichuan University, Chengdu 610041, China.
  • Xiong Q; Department of Infectious Disease, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.
  • Zheng C; Department of Microbiology, Immunology & Infection Diseases, University of Calgary, Calgary, Alberta, Canada. Electronic address: chunfu.zheng2@ucalgary.ca.
  • Yang B; Department of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu 610041, China; Sichuan Clinical Research Center for Laboratory Medicine, Chengdu 610041, China; Laboratory Medicine Research Center of West China Hospital, Sichuan University, Chengdu 610041, China. Electronic addres
  • Wang H; Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu 610041, China. Electronic address: wanghuiqing@scu.edu.cn.
Autoimmun Rev ; 23(6): 103583, 2024 Jun.
Article en En | MEDLINE | ID: mdl-39084278
ABSTRACT
T cells are key drivers of the pathogenesis of autoimmune diseases by producing cytokines, stimulating the generation of autoantibodies, and mediating tissue and cell damage. Distinct mitochondrial metabolic pathways govern the direction of T-cell differentiation and function and rely on specific nutrients and metabolic enzymes. Metabolic substrate uptake and mitochondrial metabolism form the foundational elements for T-cell activation, proliferation, differentiation, and effector function, contributing to the dynamic interplay between immunological signals and mitochondrial metabolism in coordinating adaptive immunity. Perturbations in substrate availability and enzyme activity may impair T-cell immunosuppressive function, fostering autoreactive responses and disrupting immune homeostasis, ultimately contributing to autoimmune disease pathogenesis. A growing body of studies has explored how metabolic processes regulate the function of diverse T-cell subsets in autoimmune diseases such as systemic lupus erythematosus (SLE), multiple sclerosis (MS), autoimmune hepatitis (AIH), inflammatory bowel disease (IBD), and psoriasis. This review describes the coordination of T-cell biology by mitochondrial metabolism, including the electron transport chain (ETC), oxidative phosphorylation, amino acid metabolism, fatty acid metabolism, and one­carbon metabolism. This study elucidated the intricate crosstalk between mitochondrial metabolic programs, signal transduction pathways, and transcription factors. This review summarizes potential therapeutic targets for T-cell mitochondrial metabolism and signaling in autoimmune diseases, providing insights for future studies.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Enfermedades Autoinmunes / Linfocitos T / Mitocondrias Límite: Animals / Humans Idioma: En Revista: Autoimmun Rev Asunto de la revista: ALERGIA E IMUNOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Países Bajos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Enfermedades Autoinmunes / Linfocitos T / Mitocondrias Límite: Animals / Humans Idioma: En Revista: Autoimmun Rev Asunto de la revista: ALERGIA E IMUNOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Países Bajos