Significant work from many laboratories over the last decade in the study of cancer immunology has resulted in the development of the cancer immunoediting hypothesis. This contemporary framework of the naturally arising immune system–tumor interaction is thought to comprise 3 phases: elimination, wherein immunity subserves an extrinsic tumor suppressor function and destroys nascent tumor cells; equilibrium, wherein tumor cells are constrained in a period of latency under immune control; and escape, wherein tumor cells outpace immunity and progress clinically. In this review, we address in detail the relevance of the cancer immunoediting concept to neurosurgeons and neuro-oncologists treating and studying malignant glioma by exploring the de novo immune response to these tumors, how these tumors may persist in vivo, the mechanisms by which these cells may escape/attenuate immunity, and ultimately how this concept may influence our immunotherapeutic approaches. ABBREVIATIONS: APC, antigen-presenting cell CTL, cytotoxic T lymphocyte DC, dendritic cell eGFR, endothelial growth factor receptor IL, interleukin IFN, interferon-γ MHC, major histocompatibility complex MICA/B, MHC class I chain-related A/B NK, natural killer PD-L1, programmed death receptor ligand 1 RAG2, recombinase activating gene 2 STAT3, signal transducer and activator of transcription 3 TGF-β, transforming growth factor-β TIL, tumor-infiltrating lymphocyte Treg, regulatory T cell ULBP, UL16-binding proteinSent with MobileRSS for iPhone
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