Topics
ABOUT
REVEAL IMAGESNATUREFPV

Lipid recycling by macrophage cells drives the growth of brain cancer

Sevenich, Lisa
6–8 minutes
  • NEWS AND VIEWS

In brain tumours, immune cells called macrophages scavenge lipid debris from the myelin sheath of neurons. These lipid-laden macrophages cause immunosuppression, and their transfer of lipids to tumours fuels cancer growth.

    By
  1. Lisa Sevenich

    1. Lisa Sevenich is in the Department of Neurology and Interdisciplinary Neuro-Oncology, Hertie Institute for Clinical Brain Research (HIH) and in the M3 Research Center for Malignome, Metabolome and Microbiome Research, Eberhard Karls University of Tübingen, 72076 Tübingen, Germany.

A malignant type of cancer that originates in the brain, called glioblastoma, is associated with a highly immunosuppressive microenvironment 1 . Various cues from cancer cells and their neighbours in the tumour microenvironment result in the exclusion and functional suppression of T cells — immune cells that have the potential to kill glioblastoma cells 2 , 3 . Extensive research has increased scientists’ knowledge of tumour-associated immune cells, such as microglia (the brain-resident subset of macrophages) and monocyte-derived macrophages (which are associated with cancer promotion and immunosuppression in glioblastoma) 4 – 6 . Writing in Cell , Kloosterman et al . 7 examine the broad spectrum of microglial cells and monocyte-derived macrophage populations in mouse models of glioblastoma, and provide mechanistic insights into the complex interplay between glioblastoma cells and tumour-infiltrating immune cells.

Access options

Access Nature and 54 other Nature Portfolio journals

Get Nature+, our best-value online-access subscription

$29.99 / 30 days

cancel any time

Subscribe to this journal

Receive 51 print issues and online access

$199.00 per year

only $3.90 per issue

Rent or buy this article

Prices vary by article type

from $1.95

to $39.95

Prices may be subject to local taxes which are calculated during checkout

doi: https://doi.org/10.1038/d41586-024-02868-7

References

  1. Aldape, K. et al. Nature Rev. Clin. Oncol. 16 , 509–520 (2019).

    Article PubMed Google Scholar

  2. Chongsathidkiet, P. et al. Nature Med. 24 , 1459–1468 (2018).

    Article PubMed Google Scholar

  3. Sattiraju, A. et al. Immunity 56 , 1825–1843 (2023).

    Article PubMed Google Scholar

  4. Klemm, F. et al. Cell 181 , 1643–1660 (2020).

    Article PubMed Google Scholar

  5. Ravi, V. M. et al. Cancer Cell 40 , 639–655 (2022).

    Article PubMed Google Scholar

  6. Sankowski, R. et al. Nature Med. 30 , 186–198 (2024).

    Article PubMed Google Scholar

  7. Kloosterman, D. J. et al. Cell https://doi.org/10.1016/j.cell.2024.07.030 (2024).

    Article Google Scholar

  8. Jaitin, D. A. et al. Cell 178 , 686–698 (2019).

    Article PubMed Google Scholar

  9. Xu, R. et al. Trends Endocrinol. Metab . https://doi.org/10.1016/j.tem.2024.04.009 (2024).

    Article Google Scholar

  10. Marelli, G. et al. J. Immunother. Cancer 10 , e004584 (2022).

    Article PubMed Google Scholar

  11. Grajchen, E. et al. J. Neuroinflamm. 17 , 224 (2020).

    Article Google Scholar

Download references

Competing Interests

The author declares no competing interests.

Related Articles

Subjects

Latest on: