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BACKGROUND Dysregulation of immune checkpoint molecules leads to immune evasion in human tumors but has become a viable target for tumor therapy. Here, we examined expression of LIGHT (TNFSF14), an immune checkpoint molecule, in human glioblastoma (GBM) to assess its potential as a molecular target for treatment. METHODS Molecular and clinical data from publicly available genomic databases containing WHO grade II-IV human glioma cases were analyzed. Immunohistochemistry was applied to assess LIGHT protein levels in primary tumor sections. Statistical analysis was performed using Matlab and R language. FINDINGS LIGHT was found to be elevated in aggressive gliomas, particularly in the mesenchymal molecular subtype and isocitrate dehydrogenase (IDH) wild-type GBM. LIGHT exhibited potential as a prognostic marker based on Cox regression and nomogram models. LIGHT displayed intra-tumor heterogeneity and was more highly expressed in peri-necrotic and microvascular regions. Gene ontology and pathway analysis revealed enrichment of LIGHT in multiple immune regulatory processes. Finally, in cell lineage analysis, LIGHT was found to be tightly associated with several infiltrating immune and stromal cell types which localized to the tumor microenvironment. INTERPRETATION Our data highlights the importance of LIGHT in the development of GBM and as a potential molecular target in combination with current immune checkpoint blockades for treatment of GBM.

IMMU-23. CLINICAL AND IMMUNOLOGICAL CHARACTERIZATION OF IMMUNE CHECKPOINT MOLECULE LIGHT IN HUMAN GLIOMAS