We are analyzing https://link.springer.com/article/10.1007/s11060-020-03483-y.

Title:
Immune suppression in gliomas | Journal of Neuro-Oncology
Description:
Introduction The overall survival in patients with gliomas has not significantly increased in the modern era, despite advances such as immunotherapy. This is in part due to their notorious ability to suppress local and systemic immune responses, severely restricting treatment efficacy. Methods We have reviewed the preclinical and clinical evidence for immunosuppression seen throughout the disease process in gliomas. This review aims to discuss the various ways that brain tumors, and gliomas in particular, co-opt the body’s immune system to evade detection and ensure tumor survival and proliferation. Results A multitude of mechanisms are discussed by which neoplastic cells evade detection and destruction by the immune system. These include tumor-induced T-cell and NK cell dysfunction, regulatory T-cell and myeloid-derived suppressor cell expansion, M2 phenotypic transformation in glioma-associated macrophages/microglia, upregulation of immunosuppressive glioma cell surface factors and cytokines, tumor microenvironment hypoxia, and iatrogenic sequelae of immunosuppressive treatments. Conclusions Gliomas create a profoundly immunosuppressive environment, both locally within the tumor and systemically. Future research should aim to address these immunosuppressive mechanisms in the effort to generate treatment options with meaningful survival benefits for this patient population.
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Keywords {🔍}

article, pubmed, google, scholar, cas, cells, tcell, immune, tumor, cancer, cell, patients, gliomas, central, glioma, gbm, survival, tumors, glioblastoma, immunosuppressive, expression, antigen, immunol, mechanisms, tcells, suppressor, brain, exhaustion, regulatory, shown, levels, human, tolerance, activation, peripheral, mdscs, dysfunction, myeloidderived, factors, macrophages, anergy, clin, increased, treatment, proliferation, role, exposure, phenotype, response, study,

Topics {✒️}

cd11b+cd33+hla-dr−/low cells interferon-regulatory factor/signal transducer repetitive t-cell proliferation/activation hypoxia-inducible factors hif-1α myeloid-derived suppressor cells include tumor-induced t-cell cd4 t-cell compartment article download pdf inducing t-cell suppression systemic t-cell deficits tcr t-cell receptor t-cell terminal differentiation global t-cell dysfunction normal t-cell function innate anti-tumor immunity cd4+t-cell response cd4+cd28−cd57+ t-cells cd4+cd25+foxp3+ regulatory defective ras/mapk activation suppress t-cell activation reducing t-cell output t-cell molecular states t-cell exhaustion markers circulating cd4+t-cells high-grade gliomas treated life-threatening vasogenic edema eff effector t-cell transforming growth factor-β t-cell exhaustion occurs fully functional t-cells dose-intensified temozolomide regimen reg regulatory t-cell immunologically-distinct brain prevents reduced t-cell proliferation brain tumour progression myeloid suppressor cells peripheral t-cell tolerance classical pro-inflammatory cytokine hypoxia-inducible factors ligand-expressing tumor cells age-dependent glioma mortality suppressed ifn-γ production hla-class ii molecules high-dose glucocorticoids t-cell dysfunction systemic immune responses t-cell surface [20] gliomas downregulate hla-class 25 mg/kg/day result t-cell exhaustion [16]

Questions {❓}

Moon WY, Powis SJ (2019) Does natural killer cell deficiency (NKD) increase the risk of cancer?
Strand S, Hofmann WJ, Hug H et al (1996) Lymphocyte apoptosis induced by CD95 (APO-1/Fas) ligand-expressing tumor cells—A mechanism of immune evasion?

Schema {🗺️}

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         description:The overall survival in patients with gliomas has not significantly increased in the modern era, despite advances such as immunotherapy. This is in part due to their notorious ability to suppress local and systemic immune responses, severely restricting treatment efficacy. We have reviewed the preclinical and clinical evidence for immunosuppression seen throughout the disease process in gliomas. This review aims to discuss the various ways that brain tumors, and gliomas in particular, co-opt the body’s immune system to evade detection and ensure tumor survival and proliferation. A multitude of mechanisms are discussed by which neoplastic cells evade detection and destruction by the immune system. These include tumor-induced T-cell and NK cell dysfunction, regulatory T-cell and myeloid-derived suppressor cell expansion, M2 phenotypic transformation in glioma-associated macrophages/microglia, upregulation of immunosuppressive glioma cell surface factors and cytokines, tumor microenvironment hypoxia, and iatrogenic sequelae of immunosuppressive treatments. Gliomas create a profoundly immunosuppressive environment, both locally within the tumor and systemically. Future research should aim to address these immunosuppressive mechanisms in the effort to generate treatment options with meaningful survival benefits for this patient population.
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      headline:Immune suppression in gliomas
      description:The overall survival in patients with gliomas has not significantly increased in the modern era, despite advances such as immunotherapy. This is in part due to their notorious ability to suppress local and systemic immune responses, severely restricting treatment efficacy. We have reviewed the preclinical and clinical evidence for immunosuppression seen throughout the disease process in gliomas. This review aims to discuss the various ways that brain tumors, and gliomas in particular, co-opt the body’s immune system to evade detection and ensure tumor survival and proliferation. A multitude of mechanisms are discussed by which neoplastic cells evade detection and destruction by the immune system. These include tumor-induced T-cell and NK cell dysfunction, regulatory T-cell and myeloid-derived suppressor cell expansion, M2 phenotypic transformation in glioma-associated macrophages/microglia, upregulation of immunosuppressive glioma cell surface factors and cytokines, tumor microenvironment hypoxia, and iatrogenic sequelae of immunosuppressive treatments. Gliomas create a profoundly immunosuppressive environment, both locally within the tumor and systemically. Future research should aim to address these immunosuppressive mechanisms in the effort to generate treatment options with meaningful survival benefits for this patient population.
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