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T细胞代谢作为控制β细胞自身免疫中自身反应性T细胞的靶点

T-cell Metabolism as a Target to Control Autoreactive T Cells in β-Cell Autoimmunity.

作者信息

Bordignon Carlotta, Canu Adriana, Dyczko Aleksandra, Leone Serena, Monti Paolo

机构信息

San Raffaele Diabetes Research Institute, IRCCS San Raffaele Scientific Institute, 20131, Milan, Italy.

San Raffaele Vita-Salute University, Via Olgettina 58, 20131, Milan, Italy.

出版信息

Curr Diab Rep. 2017 May;17(5):24. doi: 10.1007/s11892-017-0848-5.

DOI:10.1007/s11892-017-0848-5
PMID:28303386
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5355511/
Abstract

PURPOSE OF REVIEW

An increasing body of evidence indicates that bio-energetic metabolism of activated T cells is a potential target to control the autoimmune response in type 1 diabetes (T1D).

RECENT FINDINGS

T-cell activation and proliferation is linked to the cell capacity to provide sufficient energy and biosynthesis molecules to support T-cell growth and division. This makes T cells susceptible to metabolic inhibition for the control of the T-cell response. There is a wide therapeutic arsenal of metabolic inhibitors, including novel classes of drugs that have become recently available. With the current knowledge and availability of metabolic inhibitors, we are now in the position to design a metabolic inhibition strategy to determine whether targeting of autoreactive T cells is an effective strategy to control the process of β-cell destruction in T1D.

摘要

综述目的

越来越多的证据表明,活化T细胞的生物能量代谢是控制1型糖尿病(T1D)自身免疫反应的一个潜在靶点。

最新发现

T细胞活化和增殖与细胞提供足够能量和生物合成分子以支持T细胞生长和分裂的能力相关。这使得T细胞易受代谢抑制影响,从而控制T细胞反应。目前有大量代谢抑制剂,包括最近可用的新型药物。基于目前对代谢抑制剂的了解和可得性,我们现在有能力设计一种代谢抑制策略,以确定靶向自身反应性T细胞是否是控制T1D中β细胞破坏过程的有效策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c977/5355511/c90599e05efc/11892_2017_848_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c977/5355511/6e29f5d0298b/11892_2017_848_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c977/5355511/c90599e05efc/11892_2017_848_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c977/5355511/6e29f5d0298b/11892_2017_848_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c977/5355511/c90599e05efc/11892_2017_848_Fig2_HTML.jpg

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