IRAK4 Regulates NF-κB signaling to suppress CD8 + T cell activity and promote immune evasion in glioblastoma development.

ABSTRACT: Glioblastoma remains a highly aggressive brain tumor characterized by immune evasion, limiting the efficacy of immunotherapies. This study investigates the role of interleukin-1 receptor-associated kinase 4 (IRAK4) in modulating CD8⁺ T cell activity and immune escape in glioblastoma development. Employing high-throughput proteomics, we identified 1,205 differentially expressed proteins in glioblastoma samples, with IRAK4 significantly upregulated. Bioinformatic analyses revealed IRAK4's involvement in the nuclear factor-kappa B (NF-κB) signaling pathway, critical for immune regulation. In vitro experiments demonstrated that IRAK4 overexpression suppressed CD8⁺ T cell cytotoxicity, reducing lactate dehydrogenase release and cytokine production (interferon-gamma and tum

SUBMITTER: Xue Z 

PROVIDER: S-EPMC12847524 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature