Tumor Expression of CD83 Reduces Glioma Progression and Is Associated with Reduced Immunosuppression

Abstract

Malignant glioma, the most lethal form of brain cancer, presents with responses. Importantly, tumor-derived CD83 could mediate commuan immunosuppressive microenvironment that obstructs tumor cell nication with T cells, altering the immune microenvironment to poclearance and hampers immunotherapeutic interventions. Despite ad- tentially enhance immune-related tumor clearance. Collectively, our vancements in characterizing cellular and extracellular profiles in data suggest that tumor cell expression of CD83 supports the endogcancer, the immunosuppressive mechanisms specific to glioma remain enous antitumor T-cell constituency in malignant glioma. Future re-poorly understood. We conducted single-cell RNA sequencing of gli- search endeavors may aim to further investigate whether oma samples, which revealed a select subset of human and mouse CD83 expression can enhance immunotherapeutic approaches and glioma cells that express CD83, a marker associated with mature improve patient outcomes. antigen-presenting cells. To investigate the impact of tumor cell CD83 expression on glioma outcomes, we used an immunocompetent Significance: Immunosuppression in malignant glioma remains a mouse model of glioma, bioinformatic analyses of human samples, and barrier to therapeutic development. CD83 overexpression in human in vitro assays. Our findings revealed that CD83+ tumor cells contribute and mouse glioma increases survival. CD83+ tumor cells promote to tumor growth suppression and are associated with enhanced cyto- signatures related to cytotoxic T cells, enhanced activation of CD8+ toxic T-cell profiles and activated CD8+ T cells. Increased proin- T cells, and increased proinflammatory cytokines. These findings flammatory cytokines were identified in CD83-overexpressing tumor suggest that tumor-expressed CD83 could mediate tumor–immune conditions, which were also correlated with long-term CD8+ antitumor communications.