Colony-stimulating factors in inflammation and autoimmunity

By J. Hamilton. Nature reviews. Immunology, 2008

1,318 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/50d5faf1993730edbbc9291fdd332fb51754bb60

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In Immunology

Citations in the corpus

Bone marrow CD169+ macrophages promote the retention of hematopoietic stem and progenitor cells in the mesenchymal stem cell niche (2011, background): “Microarray expression analyses have shown that Nestin+ cells express high levels of Csf1 (Méndez-Ferrer et al., 2010b), a critical cytokine for M development and survival (Hamilton, 2008).”
Colony-stimulating factor 1 receptor (CSF1R) inhibitors in cancer therapy (2017, background): “Here, the local TME under anti-CSF1R treatment was dominated by tumor cell-derived GM-CSF and IFN-γ .”
Astrocyte crosstalk in CNS inflammation (2020, background): “GM-CSF is a known regulator of microglial activation, participating in numerous pro-inflammatory processes essential for EAE development (Hamilton, 2008; McQualter et al., 2001; Wheeler et al., 2020b).”
Macrophage plasticity and polarization in tissue repair and remodelling (2013, background): “Colony-stimulating factors are also important drivers of macrophage activation and polarization [31,32].”
Cancer-related inflammation: common themes and therapeutic opportunities. (2012, background): “M-CSF and IL-4 may underlie the proliferative apacity of macrophages including TAM [19].”
IRF5 promotes inflammatory macrophage polarization and TH1-TH17 responses (2011, background): “Plasticity and functional polarization are hallmarks of macrophages that result in the phenotypic diversity of macrophage population”
The cytokine storm in COVID-19: An overview of the involvement of the chemokine/chemokine-receptor system (2020, neutral): “These proteins are associated with inflammatory conditions and are components of an amplification cascade which ultimately increases cytokine production by macrophages at sites of inflammation, This effect perpetuates the inflammatory reaction [20].”
Oncogenic Kras-induced GM-CSF production promotes the development of pancreatic neoplasia (2012, background): “In neoplastic settings, GM-CSF has been shown to be endowed with the potential to exert both pro- and antitumorigenic effects by suppressing or enhancing tumor immunity, respectively (Hamilton, 2008).”