ArticleFrontiers in oncology2025
CD58 reshapes the immunosuppressive microenvironment in gliomas through PD-L1 upregulation.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Cluster of Differentiation 58 (CD58), a critical immune regulator, is implicated in tumor immune evasion, yet its role in remodeling the immunosuppressive microenvironment of gliomas and regulating programmed death-ligand 1 (PD-L1) remains unclear. This study aimed to elucidate the clinical and mechanistic significance of CD58 in gliomas. Methods: This study integrated bioinformatics analysis with Results: In high-grade gliomas, the expression of CD58 was significantly increased, and it showed statistical differences in relation to clinical pathological indicators. Pan-cancer analysis revealed that CD58 was associated with key immune regulatory factors, including PD-L1, chemokines (CCL5, CXCL9, CXCL10). Conclusions: CD58 drives glioma progression by upregulating PD-L1 and reshaping the tumor microenvironment toward immunosuppression. It serves as an independent prognostic biomarker and a potential therapeutic target. Targeting the CD58-PD-L1 axis may enhance immunotherapy efficacy in gliomas.
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