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Gabrusiewicz K, Rodriguez B, Wei J, et al. Glioblastoma-infiltrated innate immune cells resemble M0 macrophage phenotype. JCI Insight. 2016;1(2)doi: 10.1172/jci.insight.85841.
Gabrusiewicz, K., Rodriguez, B., Wei, J., Hashimoto, Y., Healy, L. M., Maiti, S. N., Thomas, G., Zhou, S., Wang, Q., Elakkad, A., Liebelt, B. D., Yaghi, N. K., Ezhilarasan, R., Huang, N., Weinberg, J. S., Prabhu, S. S., Rao, G., Sawaya, R., Langford, L. A., Bruner, J. M., Fuller, G. N., Bar-Or, A., Li, W., Colen, R. R., Curran, M. A., Bhat, K. P., Antel, J. P., Cooper, L. J., Sulman, E. P., & Heimberger, A. B. (2016). Glioblastoma-infiltrated innate immune cells resemble M0 macrophage phenotype. JCI insight, 1(2), . https://doi.org/10.1172/jci.insight.85841
Gabrusiewicz, Konrad, et al. "Glioblastoma-infiltrated innate immune cells resemble M0 macrophage phenotype." JCI insight vol. 1,2 (2016). doi: https://doi.org/10.1172/jci.insight.85841
Gabrusiewicz K, Rodriguez B, Wei J, Hashimoto Y, Healy LM, Maiti SN, Thomas G, Zhou S, Wang Q, Elakkad A, Liebelt BD, Yaghi NK, Ezhilarasan R, Huang N, Weinberg JS, Prabhu SS, Rao G, Sawaya R, Langford LA, Bruner JM, Fuller GN, Bar-Or A, Li W, Colen RR, Curran MA, Bhat KP, Antel JP, Cooper LJ, Sulman EP, Heimberger AB. Glioblastoma-infiltrated innate immune cells resemble M0 macrophage phenotype. JCI Insight. 2016;1(2). doi: 10.1172/jci.insight.85841. Epub 2016 Feb 25. PMID: 26973881; PMCID: PMC4784261.
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JCI Insight. 2016;1(2). doi: 10.1172/jci.insight.85841. Epub 2016 Feb 25.

Glioblastoma-infiltrated innate immune cells resemble M0 macrophage phenotype.

JCI insight

Konrad Gabrusiewicz, Benjamin Rodriguez, Jun Wei, Yuuri Hashimoto, Luke M Healy, Sourindra N Maiti, Ginu Thomas, Shouhao Zhou, Qianghu Wang, Ahmed Elakkad, Brandon D Liebelt, Nasser K Yaghi, Ravesanker Ezhilarasan, Neal Huang, Jeffrey S Weinberg, Sujit S Prabhu, Ganesh Rao, Raymond Sawaya, Lauren A Langford, Janet M Bruner, Gregory N Fuller, Amit Bar-Or, Wei Li, Rivka R Colen, Michael A Curran, Krishna P Bhat, Jack P Antel, Laurence J Cooper, Erik P Sulman, Amy B Heimberger

Affiliations

  1. Department of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
  2. Division of Biostatistics, Dan L. Duncan Cancer Center and Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA.
  3. Neuroimmunology Unit, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University, Montreal, Quebec, Canada.
  4. Division of Pediatrics.
  5. Department of Diagnostic Radiology.
  6. Department of Biostatistics.
  7. Department of Bioinformatics and Computational Biology.
  8. Department of Radiation Oncology.
  9. Department of Neuropathology.
  10. Department of Immunology, and.
  11. Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

PMID: 26973881 PMCID: PMC4784261 DOI: 10.1172/jci.insight.85841

Abstract

Glioblastomas are highly infiltrated by diverse immune cells, including microglia, macrophages, and myeloid-derived suppressor cells (MDSCs). Understanding the mechanisms by which glioblastoma-associated myeloid cells (GAMs) undergo metamorphosis into tumor-supportive cells, characterizing the heterogeneity of immune cell phenotypes within glioblastoma subtypes, and discovering new targets can help the design of new efficient immunotherapies. In this study, we performed a comprehensive battery of immune phenotyping, whole-genome microarray analysis, and microRNA expression profiling of GAMs with matched blood monocytes, healthy donor monocytes, normal brain microglia, nonpolarized M0 macrophages, and polarized M1, M2a, M2c macrophages. Glioblastoma patients had an elevated number of monocytes relative to healthy donors. Among CD11b

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