2. Academic Validation
  3. Is modulation of immune checkpoints on glioblastoma-infiltrating myeloid cells a viable therapeutic strategy?

Is modulation of immune checkpoints on glioblastoma-infiltrating myeloid cells a viable therapeutic strategy?

  • Neuro Oncol. 2025 Jan 12;27(1):33-49. doi: 10.1093/neuonc/noae193.
Ruochen Du 1 2,  Jianzhong Zhang 1 2,  Rimas V Lukas 3 1,  Shashwat Tripathi 1 2,  Jared T Ahrendsen 4 1,  Michael A Curran 5,  Crismita Dmello 1 2,  Peng Zhang 1 2,  Roger Stupp 3 1,  Ganesh Rao 6,  Amy B Heimberger 1 2
Affiliations

Affiliations

  • 1 Lou and Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
  • 2 Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
  • 3 Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
  • 4 Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA (J.T.A.).
  • 5 Department of Immunology, MD Anderson Cancer Center, the University of Texas, Houston, Texas, USA.
  • 6 Department of Neurosurgery, Baylor College of Medicine, Houston, Texas, USA.
PMID: 39427326 DOI: 10.1093/neuonc/noae193
Abstract

The field of immunology has traditionally focused on immune checkpoint modulation of adaptive immune cells. However, many malignancies such as glioblastoma are mostly devoid of T cells and rather are enriched with immunosuppressive myeloid cells of the innate immune system. While some immune checkpoint targets are shared between adaptive and innate immunity, myeloid-specific checkpoints could also serve as potential therapeutics. To better understand the impact of immune checkpoint blockade on myeloid cells, we systematically summarize the current literature focusing on the direct immunological effects of PD-L1/PD-1, CD24/Siglec-10, Collagen/LAIR-1, CX3CL1/CX3CR1, and CXCL10/CXCR3. By synthesizing the molecular mechanisms and the translational implications, we aim to prioritize agents in this category of therapeutics for glioblastoma.

Keywords

glioblastoma; immune-checkpoint blockade; myeloid cells.

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