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What is the molecular mechanism by which CD27 mediate T cell metabolism? 


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CD27 plays a crucial role in mediating T cell metabolism through various molecular mechanisms. It has been found that CD27 signaling can upregulate the expression of the antiapoptotic Bcl-x(L) protein and the Pim-1 kinase, which are essential for promoting T cell survival and clonal expansion . Additionally, CD27 signaling influences the NFkB pathway, phosphatidylinositol 3 kinase, and protein kinase B, which are involved in T cell co-activation, proliferation, and differentiation into effector and memory T cells . Furthermore, T cells can adapt their nutrient uptake and utilization to meet the energetic demands during activation and differentiation, with key molecules like AKT and AMPK regulating metabolic pathways in T cells . These findings highlight the intricate role of CD27 in regulating T cell metabolism through multiple signaling pathways.

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CD27 mediates T cell metabolism by regulating cellular signaling and transcriptional networks through metabolic sensors like AMP-mediated protein kinase, mTOR complex1, and HIF-1α, impacting T cell activation and function.
CD27 mediates T cell metabolism by promoting co-activation, proliferation, and differentiation via NFkB, phosphatidylinositol 3 kinase, and protein kinase B pathways, enhancing anti-tumor immunity.
CD27 signaling upregulates Bcl-x(L) and Pim-1 kinase expression, promoting T cell survival by antiapoptotic and prometabolic effects independent of the mTOR pathway, contributing to T cell metabolism.
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IL-27 signaling limits glycolysis in Th1 cells during infection, attenuating inflammation and immunopathology. This regulation of cellular metabolism helps control immune responses and tissue damage.

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