GBM Immunotherapy: Macrophage Impacts

ABSTRACT

Background

Glioblastoma (GBM) is an extremely aggressive form of brain tumor with low survival rates. Current treatments such as chemotherapy, radiation, and surgery are problematic due to tumor growth, invasion, and tumor microenvironment. GBM cells are resistant to these standard treatments, and the heterogeneity of the tumor makes it difficult to find a universal approach. Progression of GBM and acquisition of resistance to therapy are due to the complex interplay between tumor cells and the TME. A significant portion of the TME consists of an inflammatory infiltrate, with microglia and macrophages being the predominant cells.

Methods

Analysis of the literature data over a course of 5 years suggest that the tumor-associated macrophages (TAMs) are capable of releasing cytokines and growth factors that promote tumor proliferation, survival, and metastasis while inhibiting immune cell function at the same time.

Results

Thus, immunosuppressive state, provided with this intensively studied kind of TME cells, is supposed to promote GBM development through TAMs modulation of tumor treatment-resistance and aggressiveness. Therefore, TAMs are an attractive therapeutic target in the treatment of glioblastoma.

Conclusion

This review provides a comprehensive overview of the latest research on the nature of TAMs and the development of therapeutic strategies targeting TAMs, focusing on the variety of macrophage properties, being modulated, as well as molecular targets.

KEYWORDS:

• Glioblastoma
• immunotherapy
• macrophage
• tumor resistance

Disclosure statement

No potential conflict of interest was reported by the author(s).

Authorship contribution statement

N.L., D.A. R.K.K. and I.U. designed the study; N.L., D.A. R.K.K. and I.U. collected and analyzed the data. N.L., D.A. R.K.K. and I.U. and P.T. has been involved in drafting the manuscript and all authors have been involved in revising it critically for important intellectual content

Additional information

Funding

The author(s) reported there is no funding associated with the work featured in this article.