Coordinated regulation of myeloid cells by tumours

By D. Gabrilovich, S. Ostrand-Rosenberg, V. Bronte. Nature reviews. Immunology, 2012

3,493 citations recorded by the source corpus.

Myeloid cells are the most abundant nucleated haematopoietic cells in the human body and are a collection of distinct cell populations with many diverse functions. The three groups of terminally differentiated myeloid cells — macrophages, dendritic cells and granulocytes — are essential for the normal function of both the innate and adaptive immune systems. Mounting evidence indicates that the tumour microenvironment alters myeloid cells and can convert them into potent immunosuppressive cells. Here, we consider myeloid cells as an intricately connected, complex, single system and we focus on how tumours manipulate the myeloid system to evade the host immune response.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/991f28c968373fcf379c9c48ed9c55b046fd770c

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Citations in the corpus

Vascular normalization as an emerging strategy to enhance cancer immunotherapy (2013, neutral): “Finally, the accumulation of myeloid-derived suppressor cells (MDSC) in peripheral immune organs has been observed in both patients with cancer and tumor-bearing animals, and excess VEGF is one causative factor (21, 23).”
FAP Promotes Immunosuppression by Cancer-Associated Fibroblasts in the Tumor Microenvironment via STAT3-CCL2 Signaling. (2016, background): “Abundant presence of myeloid-origin cells, particularly myeloid-derived suppressor cells (MDSCs) including PMN-MDSCs and M-MDSCs, is a hallmark of tumor-promoting inflammation, and implicated in directly promoting tumor progression primarily by their potent immunosuppressive activities (26,27).”
Tumor-associated macrophages: from mechanisms to therapy (2014, background): “TheseM-MDSCs have greater immunosuppressive potency than the granulocytic ones and are further defined as F4/80 a marker also found on inflammatory monocytes (Gabrilovich and Nagaraj, 2009; Gabrilovich et al., 2012).”
Macrophage regulation of tumor responses to anticancer therapies. (2013, background): “TAM-mediated immunosuppression is mediated, at least in part, by induction of T cell apoptosis and nitrosylation of T cell receptors via macrophage products, like ARG1, NOS2, and peroxynitrite (Gabrilovich et al., 2012).”
A novel systemic inflammation response index (SIRI) for predicting the survival of patients with pancreatic cancer after chemotherapy (2016, background): “In the context of inflammation, neutrophil precursors, such as myelocytes and promyelocytes, might be released, thus leading to an increase in circulating granulocytes.(19) The prognostic and predictive usefulness of circulating neutrophils is apparent as an independent measure or as part of the NLR”
Targeting tumor-infiltrating macrophages decreases tumor-initiating cells, relieves immunosuppression and improves chemotherapeutic responses (2012, background): “The numbers of TAMs, G-MDSCs, inflammatory monocytes, and CD4þFOXP3þ regulatory T cells (Treg) were increased by the presence of PDAC tumors, but only TAMs increased in number following gemcitabine treatment (Fig.”
The nature of myeloid-derived suppressor cells in the tumor microenvironment (2016, background): “Hyperproduction of ROS, NO, Arg1, and inhibitory cytokines is responsible for the immune suppressive effects of MDSC (reviewed in [21]).”
Classifying cancers based on T cell infiltration and PD-L1 (2015, neutral): “In general, high den44 sities of myeloid cells, that is, macrophages and myeloid45 derived suppressor cells (MDSC), correlate with poor prognosis 47 (6).”
Tumor-Specific T Cell Dysfunction Is a Dynamic Antigen-Driven Differentiation Program Initiated Early during Tumorigenesis (2016, neutral): “…have been attributed to factors within established tumors, including the immunosuppressive microenvironment (e.g., myeloid-derived suppressor cells [Gabrilovich et al., 2012], tumor-associated macrophages [Noy and Pollard, 2014], FOXP3+ regulatory CD4+ T cells [Savage et al., 2013], IL-10, TGF-b,…”