Perspectives on Microglia-Based Immune Therapies Against Glioblastoma

Rivera, Maricruz; Bander, Evan D; Cisse, Babacar

doi:10.1016/j.wneu.2021.06.127

Cited by 6 publications

(3 citation statements)

References 42 publications

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“…Tumor-associated macrophages (TAMs) are main non-tumor cells in the tumor microenvironment (TME), which have a complex paracrine pathway with GBM cells. 83 In addition, it is confirmed that the mesenchymal phenotype and the M2 phenotype of TAMs are related significantly. 21 Not only do GBMs through paracrine pathways recruit and polarize M2 TAMs, but M2 TAMs also through paracrine pathways facilitate the malignant mesenchymal progression in GBM.…”

Section: Paracrine Pathwaysmentioning

confidence: 77%

Crosstalk between glioblastoma and tumor microenvironment drives proneural–mesenchymal transition through ligand-receptor interactions

Lai

Liao

et al. 2024

Genes & Diseases

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Section: Paracrine Pathwaysmentioning

confidence: 77%

Crosstalk between glioblastoma and tumor microenvironment drives proneural–mesenchymal transition through ligand-receptor interactions

Lai

Liao

et al. 2024

Genes & Diseases

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“…For example, M2 macrophages are particularly prominent among the infiltrating immune cells promoted by WDR76 . Alternatively, activated (M2) macrophages have been shown to promote glioma cell proliferation, elevate the expression of anti-inflammatory cytokines, and increase glioma cell invasion, ultimately leading to glioma progression and immune escape [ 40 ]. In this study, WDR76 not only contributed to the infiltration of M0 macrophages but also preferred M2 polarization, thus creating an inhibitory immune microenvironment that is more favorable for LGG progression.…”

Section: Discussionmentioning

confidence: 99%

WD repeat domain 76 predicts poor prognosis in lower grade glioma and provides an original target for immunotherapy

Cheng,

Liu,

Chang

et al. 2024

Eur J Med Res

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Background The WD40 repeat (WDR) domain provides scaffolds for numerous protein–protein interactions in multiple biological processes. WDR domain 76 (WDR76) has complex functionality owing to its diversified interactions; however, its mechanism in LGG has not yet been reported. Methods Transcriptomic data from public databases were multifariously analyzed to explore the role of WDR76 in LGG pathology and tumor immunity. Laboratory experiments were conducted to confirm these results. Results The results first confirmed that high expression of WDR76 in LGG was not only positively associated with clinical and molecular features of malignant LGG, but also served as an independent prognostic factor that predicted shorter survival in patients with LGG. Furthermore, high expression of WDR76 resulted in the upregulation of oncogenes, such as PRC1 and NUSAP1, and the activation of oncogenic mechanisms, such as the cell cycle and Notch signaling pathway. Finally, WDR76 was shown to be involved in LGG tumor immunity by promoting the infiltration of immune cells, such as M2 macrophages, and the expression of immune checkpoints, such as PDCD1 (encoding PD-1). Conclusions This study shows for the first time the diagnostic and prognostic value of WDR76 in LGG and provides a novel personalized biomarker for future targeted therapy and immunotherapy. Thus, WDR76 may significantly improve the prognosis of patients with LGG.

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“…Microglial cells within a tumor parenchyma often display a complex pattern of phenotypes, showing up-regulation of both M1 and M2 markers, with the prevalence of one phenotype on the other possibly depending on the stage of disease (Lisi et al, 2017). In light of such apparent difficulty in applying the M1/M2 paradigm to the central nervous system, it has been postulated that the notion of stimulus-dependent microglia phenotype should substitute that of microglia polarization (Rivera et al, 2021). Based on this novel paradigm, we might also conclude that hNGFp has a clear, better defined anti-inflammatory profile compared to wild type NGF.…”

Section: Discussionmentioning

confidence: 99%

The effects of painless nerve growth factor on human microglia polarization

Lisi

Marinelli²,

Ciotti³

et al. 2022

Front. Cell. Neurosci.

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Previous studies in the rat suggest that microglial cells represent a potential druggable target for nerve growth factor (NGF) in the brain. The painless human Nerve Growth Factor (hNGFp) is a recombinant mutated form of human nerve growth factor (hNGF) that shows identical neurotrophic and neuroprotective properties of wild-type NGF but displays at least 10-fold lower algogenic activity. From the pharmacological point of view, hNGFp is a biased tropomyosin receptor kinase A (TrkA) agonist and displays a significantly lower affinity for the p75 neurotrophin receptor (p75NTR). This study aimed to evaluate the expression of TrkA and p75NTR NGF receptors in two different human microglia cell lines, and to investigate the effects of hNGFp and wild-type NGF (NGF) on L-arginine metabolism, taken as a marker of microglia polarization. Both NGF receptors are expressed in human microglia cell lines and are effective in transducing signals triggered by NGF and hNGFp. The latter and, to a lesser extent, NGF inhibit cytokine-stimulated inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) production in these cells. Conversely NGF but not hNGFp stimulates arginase-mediated urea production.

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Perspectives on Microglia-Based Immune Therapies Against Glioblastoma

Cited by 6 publications

References 42 publications

Crosstalk between glioblastoma and tumor microenvironment drives proneural–mesenchymal transition through ligand-receptor interactions

Crosstalk between glioblastoma and tumor microenvironment drives proneural–mesenchymal transition through ligand-receptor interactions

WD repeat domain 76 predicts poor prognosis in lower grade glioma and provides an original target for immunotherapy

The effects of painless nerve growth factor on human microglia polarization

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