Vitamin A Metabolite Preserves T Cells’ Function as KAIST Points to a New Strategy for Treating Intractable Brain Tumors (IMAGE)
Caption
Figure 1. Mechanism of the ATRA–WNT/β-catenin–TCF-1βBD Axis
Under an exhaustion-promoting environment, CD8⁺ T cells progress to terminal exhaustion and lose their capacity to produce cytokines and cytotoxic molecules. ATRA counters this by activating WNT/β-catenin signaling within CD8⁺ T cells and increasing TCF-1βBD, a protein linked to the maintenance of T-cell function. β-catenin and TCF-1βBD then act together as transcription factors, sustaining the expression of genes associated with CD8⁺ T-cell activation. As a result, ATRA-responsive CD8⁺ T cells retain their tumor-suppressive ability even within exhaustion-promoting environments such as brain tumors, and respond more effectively to immune checkpoint inhibitors such as anti-PD-1 therapy.
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KAIST
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