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BACKGROUND: Glioblastoma (GBM) is the most prevalent and malignant primary brain tumor in adults. While immune evasion is a well-recognized driver of GBM progression and a major obstacle for efficient immunotherapy, the role of the complement system remains underexplored. C1-inhibitor (C1-INH), a regulator of complement activation, was recently found overexpressed in GBM. We therefore hypothesized
