Single-cell profiling of human gliomas reveals macrophage ontogeny as a basis for regional differences in macrophage activation in the tumor microenvironment. Müller, S., Kohanbash, G., Liu, S J., Alvarado, B., Carrera, D., Bhaduri, A., Watchmaker, P. B, Yagnik, G., Di Lullo, E., Malatesta, M., Amankulor, N. M, Kriegstein, A. R, Lim, D. A, Aghi, M., Okada, H., & Diaz, A. Genome Biol, 18(1):234, December, 2017.
abstract   bibtex   
BACKGROUND: Tumor-associated macrophages (TAMs) are abundant in gliomas and immunosuppressive TAMs are a barrier to emerging immunotherapies. It is unknown to what extent macrophages derived from peripheral blood adopt the phenotype of brain-resident microglia in pre-treatment gliomas. The relative proportions of blood-derived macrophages and microglia have been poorly quantified in clinical samples due to a paucity of markers that distinguish these cell types in malignant tissue. RESULTS: We perform single-cell RNA-sequencing of human gliomas and identify phenotypic differences in TAMs of distinct lineages. We isolate TAMs from patient biopsies and compare them with macrophages from non-malignant human tissue, glioma atlases, and murine glioma models. We present a novel signature that distinguishes TAMs by ontogeny in human gliomas. Blood-derived TAMs upregulate immunosuppressive cytokines and show an altered metabolism compared to microglial TAMs. They are also enriched in perivascular and necrotic regions. The gene signature of blood-derived TAMs, but not microglial TAMs, correlates with significantly inferior survival in low-grade glioma. Surprisingly, TAMs frequently co-express canonical pro-inflammatory (M1) and alternatively activated (M2) genes in individual cells. CONCLUSIONS: We conclude that blood-derived TAMs significantly infiltrate pre-treatment gliomas, to a degree that varies by glioma subtype and tumor compartment. Blood-derived TAMs do not universally conform to the phenotype of microglia, but preferentially express immunosuppressive cytokines and show an altered metabolism. Our results argue against status quo therapeutic strategies that target TAMs indiscriminately and in favor of strategies that specifically target immunosuppressive blood-derived TAMs.
@ARTICLE{Muller2017-zp,
  title    = "Single-cell profiling of human gliomas reveals macrophage
              ontogeny as a basis for regional differences in macrophage
              activation in the tumor microenvironment",
  author   = "M{\"u}ller, S{\"o}ren and Kohanbash, Gary and Liu, S John and
              Alvarado, Beatriz and Carrera, Diego and Bhaduri, Aparna and
              Watchmaker, Payal B and Yagnik, Garima and Di Lullo, Elizabeth
              and Malatesta, Martina and Amankulor, Nduka M and Kriegstein,
              Arnold R and Lim, Daniel A and Aghi, Manish and Okada, Hideho and
              Diaz, Aaron",
  abstract = "BACKGROUND: Tumor-associated macrophages (TAMs) are abundant in
              gliomas and immunosuppressive TAMs are a barrier to emerging
              immunotherapies. It is unknown to what extent macrophages derived
              from peripheral blood adopt the phenotype of brain-resident
              microglia in pre-treatment gliomas. The relative proportions of
              blood-derived macrophages and microglia have been poorly
              quantified in clinical samples due to a paucity of markers that
              distinguish these cell types in malignant tissue. RESULTS: We
              perform single-cell RNA-sequencing of human gliomas and identify
              phenotypic differences in TAMs of distinct lineages. We isolate
              TAMs from patient biopsies and compare them with macrophages from
              non-malignant human tissue, glioma atlases, and murine glioma
              models. We present a novel signature that distinguishes TAMs by
              ontogeny in human gliomas. Blood-derived TAMs upregulate
              immunosuppressive cytokines and show an altered metabolism
              compared to microglial TAMs. They are also enriched in
              perivascular and necrotic regions. The gene signature of
              blood-derived TAMs, but not microglial TAMs, correlates with
              significantly inferior survival in low-grade glioma.
              Surprisingly, TAMs frequently co-express canonical
              pro-inflammatory (M1) and alternatively activated (M2) genes in
              individual cells. CONCLUSIONS: We conclude that blood-derived
              TAMs significantly infiltrate pre-treatment gliomas, to a degree
              that varies by glioma subtype and tumor compartment.
              Blood-derived TAMs do not universally conform to the phenotype of
              microglia, but preferentially express immunosuppressive cytokines
              and show an altered metabolism. Our results argue against status
              quo therapeutic strategies that target TAMs indiscriminately and
              in favor of strategies that specifically target immunosuppressive
              blood-derived TAMs.",
  journal  = "Genome Biol",
  volume   =  18,
  number   =  1,
  pages    = "234",
  month    =  dec,
  year     =  2017,
  keywords = "Glioma; Immunotherapy; Macrophage; Single-cell sequencing",
  language = "en"
}

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