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通过调节 CD4T 细胞来延缓免疫衰老:一种有前途的与衰老相关疾病的治疗靶点。

Benefit delayed immunosenescence by regulating CD4T cells: A promising therapeutic target for aging-related diseases.

机构信息

Ministry of Education Key Laboratory of Pharmacology of Traditional Chinese Medical Formulae, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

State Key Laboratory of Component-Based Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

出版信息

Aging Cell. 2024 Oct;23(10):e14317. doi: 10.1111/acel.14317. Epub 2024 Aug 18.

Abstract

CD4T cells play a notable role in immune protection at different stages of life. During aging, the interaction between the body's internal and external environment and CD4T cells results in a series of changes in the CD4T cells pool making it involved in immunosenescence. Many studies have extensively examined the subsets and functionality of CD4T cells within the immune system, highlighted their pivotal role in disease pathogenesis, progression, and therapeutic interventions. However, the underlying mechanism of CD4T cells senescence and its intricate association with diseases remains to be elucidated and comprehensively understood. By summarizing the immunosenescent progress and network of CD4T cell subsets, we reveal the crucial role of CD4T cells in the occurrence and development of age-related diseases. Furthermore, we provide new insights and theoretical foundations for diseases targeting CD4T cell subsets aging as a treatment focus, offering novel approaches for therapy, especially in infections, cancers, autoimmune diseases, and other diseases in the elderly.

摘要

CD4T 细胞在生命的不同阶段发挥着重要的免疫保护作用。在衰老过程中,机体的内、外环境与 CD4T 细胞相互作用,导致 CD4T 细胞库发生一系列变化,从而参与免疫衰老。许多研究广泛研究了免疫系统中 CD4T 细胞亚群的亚群和功能,强调了它们在疾病发病机制、进展和治疗干预中的关键作用。然而,CD4T 细胞衰老的潜在机制及其与疾病的复杂关联仍有待阐明和全面理解。通过总结 CD4T 细胞亚群的免疫衰老进展和网络,我们揭示了 CD4T 细胞在与年龄相关的疾病发生和发展中的关键作用。此外,我们为以 CD4T 细胞亚群衰老为治疗重点的疾病提供了新的见解和理论基础,为治疗,特别是感染、癌症、自身免疫性疾病和老年人的其他疾病提供了新的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a47d/11464113/064ac2312627/ACEL-23-e14317-g001.jpg

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