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GM-CSF in inflammation

Hamilton, John A.·2020·Journal of Experimental Medicine
DOI 10.1084/jem.20190945PMC PMC7037240
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Abstract

Granulocyte–macrophage colony-stimulating factor (GM-CSF) has many more functions than its original in vitro identification as an inducer of granulocyte and macrophage development from progenitor cells. Key features of GM-CSF biology need to be defined better, such as the responding and producing cell types, its links with other mediators, its prosurvival versus activation/differentiation functions, and when it is relevant in pathology. Significant preclinical data have emerged from GM-CSF deletion/depletion approaches indicating that GM-CSF is a potential target in many inflammatory/autoimmune conditions. Clinical trials targeting GM-CSF or its receptor have shown encouraging efficacy and safety profiles, particularly in rheumatoid arthritis. This review provides an update on the above topics and current issues/questions surrounding GM-CSF biology.

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Figure 1. A GM-CSF–IRF4–CCL17 pathway in inflammation and pain. During an inflammatory reaction, GM-CSF, generated following TNF-dependent and -independent stimulation, induces in monocytes and macrophages the formation of CCL17 through a signaling pathway involving the induction of the transcription factor, IRF4, via the activity of the demethylase, JMJD3 (Achuthan et al., 2016). By unknown mechanisms, secreted CCL17 can result in inflammation and tissue remodeling, for example, in arthritic joints, as well as drive the development of pain; the latter response appears to require a contribution from an eicosanoid (for example, PGE2). GM-CSF–IRF4 signaling can in addition control expression in monocytes and macrophages of other potential proinflammatory effectors, such as surface-bound MHC class II. GM-CSF and TNF, potentially produced by numerous cell types (not shown) in response to various stimuli, including damage-associated molecular patterns (DAMPs), can engage in a cytokine loop, thus potentially linking TNF biology to the GM-CSF–CCL17 pathway (Cook et al., 2018b).
Figure 1. A GM-CSF–IRF4–CCL17 pathway in inflammation and pain. During an inflammatory reaction, GM-CSF, generated following TNF-dependent and -independent stimulation, induces in monocytes and macrophages the formation of CCL17 through a signaling pathway involving the induction of the transcription factor, IRF4, via the activity of the demethylase, JMJD3 (Achuthan et al., 2016). By unknown mechanisms, secreted CCL17 can result in inflammation and tissue remodeling, for example, in arthritic joints, as well as drive the development of pain; the latter response appears to require a contribution from an eicosanoid (for example, PGE2). GM-CSF–IRF4 signaling can in addition control expression in monocytes and macrophages of other potential proinflammatory effectors, such as surface-bound MHC class II. GM-CSF and TNF, potentially produced by numerous cell types (not shown) in response to various stimuli, including damage-associated molecular patterns (DAMPs), can engage in a cytokine loop, thus potentially linking TNF biology to the GM-CSF–CCL17 pathway (Cook et al., 2018b).CC BY-NC-SA · PubMed Central
Figure 2. GM-CSF and control of target cell numbers and function in inflammation. During an inflammatory reaction, it is likely that the major actions of endogenous GM-CSF are in the inflamed tissue in which GM-CSF can act in a concentration-dependent manner on resident macrophages and/or migrated monocytes, neutrophils, and eosinophils to promote their survival and/or modify their differentiation/polarization, such as the maturation of the monocytes into MoDCs and macrophages. Myeloid cell trafficking in (or out) of the inflamed tissue may also be under GM-CSF control. The cell differentiation/polarization can be characterized by the production of proinflammatory mediators such as cytokines, chemokines, proteases, reactive oxygen species, etc. (not shown); monocyte/macrophages may also proliferate (not shown). The tissue-derived GM-CSF may also act systemically in the blood and/or bone marrow, either directly or indirectly via its cellular targets in the tissue (not shown), to activate myeloid cells in the blood before their migration into the inflamed tissue and contribute to this migration; it may contribute as well as to myeloid mobilization/cell migration from the bone marrow, where it may also promote lineage-specific myelopoiesis from progenitor cells. Whether the particular highlighted actions of GM-CSF operate is currently debated and is likely to depend on the nature of the inflammatory reaction and the levels of GM-CSF attained from hemopoietic (e.g., lymphocyte) and nonhemopoietic (e.g., fibroblast) cell populations. GM-CSF targeting (depicted by inhibitory lines) could occur locally in the inflamed tissue and systemically to control disease.
Figure 2. GM-CSF and control of target cell numbers and function in inflammation. During an inflammatory reaction, it is likely that the major actions of endogenous GM-CSF are in the inflamed tissue in which GM-CSF can act in a concentration-dependent manner on resident macrophages and/or migrated monocytes, neutrophils, and eosinophils to promote their survival and/or modify their differentiation/polarization, such as the maturation of the monocytes into MoDCs and macrophages. Myeloid cell trafficking in (or out) of the inflamed tissue may also be under GM-CSF control. The cell differentiation/polarization can be characterized by the production of proinflammatory mediators such as cytokines, chemokines, proteases, reactive oxygen species, etc. (not shown); monocyte/macrophages may also proliferate (not shown). The tissue-derived GM-CSF may also act systemically in the blood and/or bone marrow, either directly or indirectly via its cellular targets in the tissue (not shown), to activate myeloid cells in the blood before their migration into the inflamed tissue and contribute to this migration; it may contribute as well as to myeloid mobilization/cell migration from the bone marrow, where it may also promote lineage-specific myelopoiesis from progenitor cells. Whether the particular highlighted actions of GM-CSF operate is currently debated and is likely to depend on the nature of the inflammatory reaction and the levels of GM-CSF attained from hemopoietic (e.g., lymphocyte) and nonhemopoietic (e.g., fibroblast) cell populations. GM-CSF targeting (depicted by inhibitory lines) could occur locally in the inflamed tissue and systemically to control disease.CC BY-NC-SA · PubMed Central

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Research works printed but not linked: 202

  1. Achuthan, 2016, Granulocyte macrophage colony-stimulating factor induces CCL17 production via IRF4 to mediate inflammation, J. Clin. Invest., 126, 3453, 10.1172/JCI87828 · DOI
  2. Achuthan, 2018, Glucocorticoids promote apoptosis of proinflammatory monocytes by inhibiting ERK activity, Cell Death Dis., 9, 267, 10.1038/s41419-018-0332-4 · DOI
  3. Alferink, 2003, Compartmentalized production of CCL17 in vivo: strong inducibility in peripheral dendritic cells contrasts selective absence from the spleen, J. Exp. Med., 197, 585, 10.1084/jem.20021859 · DOI
  4. Al-Mossawi, 2017, Unique transcriptome signatures and GM-CSF expression in lymphocytes from patients with spondyloarthritis, Nat. Commun., 8, 1510, 10.1038/s41467-017-01771-2 · DOI
  5. Alnek, 2015, Increased Blood Levels of Growth Factors, Proinflammatory Cytokines, and Th17 Cytokines in Patients with Newly Diagnosed Type 1 Diabetes, PLoS One., 10, 10.1371/journal.pone.0142976 · DOI
  6. Alvaro-Gracia, 1989, Cytokines in chronic inflammatory arthritis. IV. Granulocyte/macrophage colony-stimulating factor-mediated induction of class II MHC antigen on human monocytes: a possible role in rheumatoid arthritis, J. Exp. Med., 170, 865, 10.1084/jem.170.3.865 · DOI
  7. Andtbacka, 2015, Talimogene Laherparepvec Improves Durable Response Rate in Patients With Advanced Melanoma, J. Clin. Oncol., 33, 2780, 10.1200/JCO.2014.58.3377 · DOI
  8. Anzai, 2017, The infarcted myocardium solicits GM-CSF for the detrimental oversupply of inflammatory leukocytes, J. Exp. Med., 214, 3293, 10.1084/jem.20170689 · DOI
  9. Bali, 2013, Transcriptional mechanisms underlying sensitization of peripheral sensory neurons by granulocyte-/granulocyte-macrophage colony stimulating factors, Mol. Pain., 9, 48, 10.1186/1744-8069-9-48 · DOI
  10. Becher, 2016, GM-CSF: From Growth Factor to Central Mediator of Tissue Inflammation, Immunity., 45, 963, 10.1016/j.immuni.2016.10.026 · DOI
  11. Bhattacharya, 2015, GM-CSF: An immune modulatory cytokine that can suppress autoimmunity, Cytokine., 75, 261, 10.1016/j.cyto.2015.05.030 · DOI
  12. Bischof, 2000, Exacerbation of acute inflammatory arthritis by the colony-stimulating factors CSF-1 and granulocyte macrophage (GM)-CSF: evidence of macrophage infiltration and local proliferation, Clin. Exp. Immunol., 119, 361, 10.1046/j.1365-2249.2000.01125.x · DOI
  13. Borriello, 2017, GM-CSF and IL-3 Modulate Human Monocyte TNF-α Production and Renewal in In Vitro Models of Trained Immunity, Front. Immunol., 7, 680, 10.3389/fimmu.2016.00680 · DOI
  14. Bozinovski, 2002, Granulocyte/macrophage-colony-stimulating factor (GM-CSF) regulates lung innate immunity to lipopolysaccharide through Akt/Erk activation of NFkappa B and AP-1 in vivo, J. Biol. Chem., 277, 42808, 10.1074/jbc.M207840200 · DOI
  15. Broughton, 2016, Conformational changes in the GM-CSF receptor suggest a molecular mechanism for affinity conversion and receptor signaling, Structure., 24, 1271, 10.1016/j.str.2016.05.017 · DOI
  16. Burgess, 1980, The nature and action of granulocyte-macrophage colony stimulating factors, Blood., 56, 947, 10.1182/blood.V56.6.947.947 · DOI
  17. Burmester, 2011, Mavrilimumab, a human monoclonal antibody targeting GM-CSF receptor-α, in subjects with rheumatoid arthritis: a randomised, double-blind, placebo-controlled, phase I, first-in-human study, Ann. Rheum. Dis., 70, 1542, 10.1136/ard.2010.146225 · DOI
  18. Burmester, 2013, Tofacitinib (CP-690,550) in combination with methotrexate in patients with active rheumatoid arthritis with an inadequate response to tumour necrosis factor inhibitors: a randomised phase 3 trial, Lancet., 381, 451, 10.1016/S0140-6736(12)61424-X · DOI
  19. Burmester, 2017, A randomised phase IIb study of mavrilimumab, a novel GM-CSF receptor alpha monoclonal antibody, in the treatment of rheumatoid arthritis, Ann. Rheum. Dis., 76, 1020, 10.1136/annrheumdis-2016-210624 · DOI
  20. Burmester, 2018, Mavrilimumab, a Fully Human Granulocyte-Macrophage Colony-Stimulating Factor Receptor α Monoclonal Antibody: Long-Term Safety and Efficacy in Patients With Rheumatoid Arthritis, Arthritis Rheumatol., 70, 679, 10.1002/art.40420 · DOI
  21. Campbell, 1997, Granulocyte-macrophage colony stimulating factor exacerbates collagen induced arthritis in mice, Ann. Rheum. Dis., 56, 364, 10.1136/ard.56.6.364 · DOI
  22. Campbell, 1998, Protection from collagen-induced arthritis in granulocyte-macrophage colony-stimulating factor-deficient mice, J. Immunol., 161, 3639, 10.4049/jimmunol.161.7.3639 · DOI
  23. Campbell, 2011, Differentiation of inflammatory dendritic cells is mediated by NF-κB1-dependent GM-CSF production in CD4 T cells, J. Immunol., 186, 5468, 10.4049/jimmunol.1002923 · DOI
  24. Carbajal, 2015, Th Cell Diversity in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis, J. Immunol., 195, 2552, 10.4049/jimmunol.1501097 · DOI
  25. Carrieri, 1998, Profile of cerebrospinal fluid and serum cytokines in patients with relapsing-remitting multiple sclerosis: a correlation with clinical activity, Immunopharmacol. Immunotoxicol., 20, 373, 10.3109/08923979809034820 · DOI
  26. Cates, 2004, Intranasal exposure of mice to house dust mite elicits allergic airway inflammation via a GM-CSF-mediated mechanism, J. Immunol., 173, 6384, 10.4049/jimmunol.173.10.6384 · DOI
  27. Chow, 2016, Innate Allorecognition Results in Rapid Accumulation of Monocyte-Derived Dendritic Cells, J. Immunol., 197, 2000, 10.4049/jimmunol.1600181 · DOI
  28. Cohen, 2018, Lung Single-Cell Signaling Interaction Map Reveals Basophil Role in Macrophage Imprinting, Cell., 175, 1031, 10.1016/j.cell.2018.09.009 · DOI
  29. Constantinescu, 2015, Randomized phase 1b trial of MOR103, a human antibody to GM-CSF, in multiple sclerosis, Neurol. Neuroimmunol. Neuroinflamm., 2, 10.1212/NXI.0000000000000117 · DOI
  30. Conti, 2008, GM-CSF in the generation of dendritic cells from human blood monocyte precursors: recent advances, Immunobiology., 213, 859, 10.1016/j.imbio.2008.07.017 · DOI
  31. Cook, 2018, Investigational therapies targeting the granulocyte macrophage colony-stimulating factor receptor-α in rheumatoid arthritis: focus on mavrilimumab, Ther. Adv. Musculoskelet. Dis., 10, 29, 10.1177/1759720X17752036 · DOI
  32. Cook, 2001, Blockade of collagen-induced arthritis post-onset by antibody to granulocyte-macrophage colony-stimulating factor (GM-CSF): requirement for GM-CSF in the effector phase of disease, Arthritis Res., 3, 293, 10.1186/ar318 · DOI
  33. Cook, 2003, The phenotype of inflammatory macrophages is stimulus dependent: implications for the nature of the inflammatory response, J. Immunol., 171, 4816, 10.4049/jimmunol.171.9.4816 · DOI
  34. Cook, 2004, Stimulus-dependent requirement for granulocyte-macrophage colony-stimulating factor in inflammation, J. Immunol., 173, 4643, 10.4049/jimmunol.173.7.4643 · DOI
  35. Cook, 2011, Regulation of systemic and local myeloid cell subpopulations by bone marrow cell-derived granulocyte-macrophage colony-stimulating factor in experimental inflammatory arthritis, Arthritis Rheum., 63, 2340, 10.1002/art.30354 · DOI
  36. Cook, 2013, Granulocyte-macrophage colony-stimulating factor is a key mediator in inflammatory and arthritic pain, Ann. Rheum. Dis., 72, 265, 10.1136/annrheumdis-2012-201703 · DOI
  37. Cook, 2016, Granulocyte macrophage colony-stimulating factor receptor α expression and its targeting in antigen-induced arthritis and inflammation, Arthritis Res. Ther., 18, 287, 10.1186/s13075-016-1185-9 · DOI
  38. Cook, 2018, Immune Cytokines and Their Receptors in Inflammatory Pain, Trends Immunol., 39, 240, 10.1016/j.it.2017.12.003 · DOI
  39. Cook, 2018, TNF and granulocyte macrophage-colony stimulating factor interdependence mediates inflammation via CCL17, JCI Insight., 3, 10.1172/jci.insight.99249 · DOI
  40. Cowburn, 2011, Granulocyte/macrophage colony-stimulating factor causes a paradoxical increase in the BH3-only pro-apoptotic protein Bim in human neutrophils, Am. J. Respir. Cell Mol. Biol., 44, 879, 10.1165/rcmb.2010-0101OC · DOI
  41. Croxford, 2015, The Cytokine GM-CSF Drives the Inflammatory Signature of CCR2+ Monocytes and Licenses Autoimmunity, Immunity., 43, 502, 10.1016/j.immuni.2015.08.010 · DOI · Paper page
  42. Croxford, 2015, GM-CSF in Neuroinflammation: Licensing Myeloid Cells for Tissue Damage, Trends Immunol., 36, 651, 10.1016/j.it.2015.08.004 · DOI
  43. Curran, 2012, Lactoferrin regulates an axis involving CD11b and CD49d integrins and the chemokines MIP-1α and MCP-1 in GM-CSF-treated human primary eosinophils, J. Interferon Cytokine Res., 32, 450, 10.1089/jir.2011.0111 · DOI
  44. Däbritz, 2014, Granulocyte macrophage colony-stimulating factor and the intestinal innate immune cell homeostasis in Crohn’s disease, Am. J. Physiol. Gastrointest. Liver Physiol., 306, G455, 10.1152/ajpgi.00409.2013 · DOI
  45. Däbritz, 2015, GM-CSF and the role of myeloid regulatory cells in the pathogenesis and treatment of Crohn’s disease, Mol. Cell Pediatr., 2, 12, 10.1186/s40348-015-0024-4 · DOI
  46. Ditiatkovski, 2006, GM-CSF deficiency reduces macrophage PPAR-gamma expression and aggravates atherosclerosis in ApoE-deficient mice, Arterioscler. Thromb. Vasc. Biol., 26, 2337, 10.1161/01.ATV.0000238357.60338.90 · DOI
  47. Dohlman, 2017, T Cell-Derived Granulocyte-Macrophage Colony-Stimulating Factor Contributes to Dry Eye Disease Pathogenesis by Promoting CD11b+ Myeloid Cell Maturation and Migration, Invest. Ophthalmol. Vis. Sci., 58, 1330, 10.1167/iovs.16-20789 · DOI
  48. Dougan, 2019, GM-CSF, IL-3, and IL-5 Family of Cytokines: Regulators of Inflammation, Immunity., 50, 796, 10.1016/j.immuni.2019.03.022 · DOI
  49. Dranoff, 1993, Vaccination with irradiated tumor cells engineered to secrete murine granulocyte-macrophage colony-stimulating factor stimulates potent, specific, and long-lasting anti-tumor immunity, Proc. Natl. Acad. Sci. USA., 90, 3539, 10.1073/pnas.90.8.3539 · DOI
  50. Dranoff, 1994, Involvement of granulocyte-macrophage colony-stimulating factor in pulmonary homeostasis, Science., 264, 713, 10.1126/science.8171324 · DOI
  51. Edelson, 2011, Batf3-dependent CD11b(low/-) peripheral dendritic cells are GM-CSF-independent and are not required for Th cell priming after subcutaneous immunization, PLoS One., 6, 10.1371/journal.pone.0025660 · DOI
  52. Egea, 2010, GM-CSF: a role in immune and inflammatory reactions in the intestine, Expert Rev. Gastroenterol. Hepatol., 4, 723, 10.1586/egh.10.73 · DOI
  53. Eguchi, 2013, Interferon regulatory factor 4 regulates obesity-induced inflammation through regulation of adipose tissue macrophage polarization, Diabetes., 62, 3394, 10.2337/db12-1327 · DOI
  54. Enzler, 2003, Deficiencies of GM-CSF and interferon gamma link inflammation and cancer, J. Exp. Med., 197, 1213, 10.1084/jem.20021258 · DOI
  55. Erlich, 2019, Macrophages, rather than DCs, are responsible for inflammasome activity in the GM-CSF BMDC model, Nat. Immunol., 20, 397, 10.1038/s41590-019-0313-5 · DOI
  56. Etemad, 2012, A novel in vitro human microglia model: characterization of human monocyte-derived microglia, J. Neurosci. Methods., 209, 79, 10.1016/j.jneumeth.2012.05.025 · DOI
  57. Fleetwood, 2005, Functions of granulocyte-macrophage colony-stimulating factor, Crit. Rev. Immunol., 25, 405, 10.1615/CritRevImmunol.v25.i5.50 · DOI
  58. Fleetwood, 2007, Granulocyte-macrophage colony-stimulating factor (CSF) and macrophage CSF-dependent macrophage phenotypes display differences in cytokine profiles and transcription factor activities: implications for CSF blockade in inflammation, J. Immunol., 178, 5245, 10.4049/jimmunol.178.8.5245 · DOI · Paper page
  59. Ganesh, 2009, GM-CSF-induced CD11c+CD8a--dendritic cells facilitate Foxp3+ and IL-10+ regulatory T cell expansion resulting in suppression of autoimmune thyroiditis, Int. Immunol., 21, 269, 10.1093/intimm/dxn147 · DOI
  60. Gao, 2013, Control of T helper 2 responses by transcription factor IRF4-dependent dendritic cells, Immunity., 39, 722, 10.1016/j.immuni.2013.08.028 · DOI
  61. Gathungu, 2013, Granulocyte-macrophage colony-stimulating factor autoantibodies: a marker of aggressive Crohn’s disease, Inflamm. Bowel Dis., 19, 1671, 10.1097/MIB.0b013e318281f506 · DOI
  62. Goldmann, 2013, The expanding world of extracellular traps: not only neutrophils but much more, Front. Immunol., 3, 420, 10.3389/fimmu.2012.00420 · DOI
  63. Greven, 2015, Preclinical characterisation of the GM-CSF receptor as a therapeutic target in rheumatoid arthritis, Ann. Rheum. Dis., 74, 1924, 10.1136/annrheumdis-2014-205234 · DOI
  64. Grifka-Walk, 2015, IL-12-polarized Th1 cells produce GM-CSF and induce EAE independent of IL-23, Eur. J. Immunol., 45, 2780, 10.1002/eji.201545800 · DOI
  65. Griseri, 2012, Dysregulated hematopoietic stem and progenitor cell activity promotes interleukin-23-driven chronic intestinal inflammation, Immunity., 37, 1116, 10.1016/j.immuni.2012.08.025 · DOI
  66. Griseri, 2015, Granulocyte Macrophage Colony-Stimulating Factor-Activated Eosinophils Promote Interleukin-23 Driven Chronic Colitis, Immunity., 43, 187, 10.1016/j.immuni.2015.07.008 · DOI
  67. Guo, 2018, Blockade of GM-CSF pathway induced sustained suppression of myeloid and T cell activities in rheumatoid arthritis, Rheumatology (Oxford)., 57, 175, 10.1093/rheumatology/kex383 · DOI
  68. Guo, 2019, Pharmacodynamic biomarkers and differential effects of TNF- and GM-CSF-targeting biologics in rheumatoid arthritis, Int. J. Rheum. Dis., 22, 646, 10.1111/1756-185X.13395 · DOI
  69. Hamilton, 1993, A colony-stimulating factor network involving mononuclear phagocytes and other cells, 29, 10.1159/000422228 · DOI
  70. Hamilton, 1993, Rheumatoid arthritis: opposing actions of haemopoietic growth factors and slow-acting anti-rheumatic drugs, Lancet., 342, 536, 10.1016/0140-6736(93)91653-4 · DOI
  71. Hamilton, 1994, Coordinate and noncoordinate colony stimulating factor formation by human monocytes, J. Leukoc. Biol., 55, 355, 10.1002/jlb.55.3.355 · DOI
  72. Hamilton, 2002, GM-CSF in inflammation and autoimmunity, Trends Immunol., 23, 403, 10.1016/S1471-4906(02)02260-3 · DOI
  73. Hamilton, 2015, GM-CSF as a target in inflammatory/autoimmune disease: current evidence and future therapeutic potential, Expert Rev. Clin. Immunol., 11, 457, 10.1586/1744666X.2015.1024110 · DOI
  74. Hamilton, 2013, Colony stimulating factors and myeloid cell biology in health and disease, Trends Immunol., 34, 81, 10.1016/j.it.2012.08.006 · DOI · Paper page
  75. Hamilton, 2009, The dynamics of macrophage lineage populations in inflammatory and autoimmune diseases, Arthritis Rheum., 60, 1210, 10.1002/art.24505 · DOI
  76. Hamilton, 1980, Stimulation of macrophage plasminogen activator activity by colony-stimulating factors, J. Cell. Physiol., 103, 435, 10.1002/jcp.1041030309 · DOI
  77. Hamilton, 2017, Anti-colony-stimulating factor therapies for inflammatory and autoimmune diseases, Nat. Rev. Drug Discov., 16, 53, 10.1038/nrd.2016.231 · DOI
  78. Handman, 1979, Stimulation by granulocyte-macrophage colony-stimulating factor of Leishmania tropica killing by macrophages, J. Immunol., 122, 1134, 10.4049/jimmunol.122.3.1134 · DOI
  79. Hansen, 2008, The structure of the GM-CSF receptor complex reveals a distinct mode of cytokine receptor activation, Cell., 134, 496, 10.1016/j.cell.2008.05.053 · DOI
  80. Hart, 1988, Synergistic activation of human monocytes by granulocyte-macrophage colony-stimulating factor and IFN-gamma. Increased TNF-alpha but not IL-1 activity, J. Immunol., 141, 1516, 10.4049/jimmunol.141.5.1516 · DOI
  81. Hazenberg, 1989, Correction of granulocytopenia in Felty’s syndrome by granulocyte-macrophage colony-stimulating factor. Simultaneous induction of interleukin-6 release and flare-up of the arthritis, Blood., 74, 2769, 10.1182/blood.V74.8.2769.2769 · DOI
  82. Heiseke, 2012, CCL17 promotes intestinal inflammation in mice and counteracts regulatory T cell-mediated protection from colitis, Gastroenterology., 142, 335, 10.1053/j.gastro.2011.10.027 · DOI
  83. Helft, 2015, GM-CSF Mouse Bone Marrow Cultures Comprise a Heterogeneous Population of CD11c(+)MHCII(+) Macrophages and Dendritic Cells, Immunity., 42, 1197, 10.1016/j.immuni.2015.05.018 · DOI
  84. Hilgendorf, 2014, Innate response activator B cells aggravate atherosclerosis by stimulating T helper-1 adaptive immunity, Circulation., 129, 1677, 10.1161/CIRCULATIONAHA.113.006381 · DOI
  85. Hirota, 2018, Autoimmune Th17 Cells Induced Synovial Stromal and Innate Lymphoid Cell Secretion of the Cytokine GM-CSF to Initiate and Augment Autoimmune Arthritis, Immunity., 48, 1220, 10.1016/j.immuni.2018.04.009 · DOI
  86. Hodi, 2014, Ipilimumab plus sargramostim vs ipilimumab alone for treatment of metastatic melanoma: a randomized clinical trial, JAMA., 312, 1744, 10.1001/jama.2014.13943 · DOI
  87. Honma, 2005, Interferon regulatory factor 4 negatively regulates the production of proinflammatory cytokines by macrophages in response to LPS, Proc. Natl. Acad. Sci. USA., 102, 16001, 10.1073/pnas.0504226102 · DOI
  88. Hornell, 2003, Regulation of the class II MHC pathway in primary human monocytes by granulocyte-macrophage colony-stimulating factor, J. Immunol., 171, 2374, 10.4049/jimmunol.171.5.2374 · DOI
  89. Hu, 2019, Interleukin-1β-induced IRAK1 ubiquitination is required for TH-GM-CSF cell differentiation in T cell-mediated inflammation, J. Autoimmun., 102, 50, 10.1016/j.jaut.2019.04.010 · DOI
  90. Huizinga, 2017, Phase 1b randomized, double-blind study of namilumab, an anti-granulocyte macrophage colony-stimulating factor monoclonal antibody, in mild-to-moderate rheumatoid arthritis, Arthritis Res. Ther., 19, 53, 10.1186/s13075-017-1267-3 · DOI
  91. Iellem, 2001, Unique chemotactic response profile and specific expression of chemokine receptors CCR4 and CCR8 by CD4(+)CD25(+) regulatory T cells, J. Exp. Med., 194, 847, 10.1084/jem.194.6.847 · DOI
  92. Ifergan, 2017, Targeting the GM-CSF receptor for the treatment of CNS autoimmunity, J. Autoimmun., 84, 1, 10.1016/j.jaut.2017.06.005 · DOI
  93. Ina, 1999, Increased mucosal production of granulocyte colony-stimulating factor is related to a delay in neutrophil apoptosis in Inflammatory Bowel disease, J. Gastroenterol. Hepatol., 14, 46, 10.1046/j.1440-1746.1999.01807.x · DOI
  94. Inaba, 1992, Generation of large numbers of dendritic cells from mouse bone marrow cultures supplemented with granulocyte/macrophage colony-stimulating factor, J. Exp. Med., 176, 1693, 10.1084/jem.176.6.1693 · DOI
  95. Izquierdo, 2015, Reshaping of Human Macrophage Polarization through Modulation of Glucose Catabolic Pathways, J. Immunol., 195, 2442, 10.4049/jimmunol.1403045 · DOI
  96. Jiao, 2014, The closely related CD103+ dendritic cells (DCs) and lymphoid-resident CD8+ DCs differ in their inflammatory functions, PLoS One., 9, 10.1371/journal.pone.0091126 · DOI
  97. Kabat, 2016, The autophagy gene Atg16l1 differentially regulates Treg and TH2 cells to control intestinal inflammation, eLife., 5, 10.7554/eLife.12444 · DOI · Paper page
  98. Kasinrerk, 1993, CD1 molecule expression on human monocytes induced by granulocyte-macrophage colony-stimulating factor, J. Immunol., 150, 579, 10.4049/jimmunol.150.2.579 · DOI
  99. Kelso, 2015, Granulocyte-macrophage colony stimulating factor exerts protective and immunomodulatory effects in cortical trauma, J. Neuroimmunol., 278, 162, 10.1016/j.jneuroim.2014.11.002 · DOI
  100. Khajah, 2011, Granulocyte-macrophage colony-stimulating factor (GM-CSF): a chemoattractive agent for murine leukocytes in vivo, J. Leukoc. Biol., 89, 945, 10.1189/jlb.0809546 · DOI
  101. Kim, 2018, Dysregulated IL-1β-GM-CSF Axis in Acute Rheumatic Fever That Is Limited by Hydroxychloroquine, Circulation., 138, 2648, 10.1161/CIRCULATIONAHA.118.033891 · DOI
  102. King, 2009, Circulating Ly-6C+ myeloid precursors migrate to the CNS and play a pathogenic role during autoimmune demyelinating disease, Blood., 113, 3190, 10.1182/blood-2008-07-168575 · DOI · Paper page
  103. King, 2010, GM-CSF-dependent, CD103+ dermal dendritic cells play a critical role in Th effector cell differentiation after subcutaneous immunization, J. Exp. Med., 207, 953, 10.1084/jem.20091844 · DOI
  104. Kitching, 2002, The requirement for granulocyte-macrophage colony-stimulating factor and granulocyte colony-stimulating factor in leukocyte-mediated immune glomerular injury, J. Am. Soc. Nephrol., 13, 350, 10.1681/ASN.V132350 · DOI
  105. Knoop, 2018, GM-CSF producing autoreactive CD4+ T cells in type 1 diabetes, Clin. Immunol., 188, 23, 10.1016/j.clim.2017.12.002 · DOI
  106. Ko, 2014, GM-CSF-responsive monocyte-derived dendritic cells are pivotal in Th17 pathogenesis, J. Immunol., 192, 2202, 10.4049/jimmunol.1302040 · DOI
  107. Korzenik, 2007, Is Crohn’s disease due to defective immunity?, Gut., 56, 2, 10.1136/gut.2006.095588 · DOI
  108. Krausgruber, 2011, IRF5 promotes inflammatory macrophage polarization and TH1-TH17 responses, Nat. Immunol., 12, 231, 10.1038/ni.1990 · DOI
  109. Kwon, 2018, IL-17A+GM-CSF+ Neutrophils Are the Major Infiltrating Cells in Interstitial Lung Disease in an Autoimmune Arthritis Model, Front. Immunol., 9, 1544, 10.3389/fimmu.2018.01544 · DOI
  110. Lacey, 2012, Defining GM-CSF- and macrophage-CSF-dependent macrophage responses by in vitro models, J. Immunol., 188, 5752, 10.4049/jimmunol.1103426 · DOI
  111. Lam, 2015, GM-CSF and uPA are required for Porphyromonas gingivalis-induced alveolar bone loss in a mouse periodontitis model, Immunol. Cell Biol., 93, 705, 10.1038/icb.2015.25 · DOI
  112. Lari, 2007, Macrophage lineage phenotypes and osteoclastogenesis--complexity in the control by GM-CSF and TGF-beta, Bone., 40, 323, 10.1016/j.bone.2006.09.003 · DOI
  113. Lee, 2018, CCL17 blockade as a therapy for osteoarthritis pain and disease, Arthritis Res. Ther., 20, 62, 10.1186/s13075-018-1560-9 · DOI
  114. Lee, 2019, GM-CSF- and IRF4-Dependent Signaling Can Regulate Myeloid Cell Numbers and the Macrophage Phenotype during Inflammation, J. Immunol., 202, 3033, 10.4049/jimmunol.1801549 · DOI
  115. Lehtonen, 2002, Granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced STAT5 activation and target-gene expression during human monocyte/macrophage differentiation, J. Leukoc. Biol., 71, 511, 10.1189/jlb.71.3.511 · DOI
  116. Lehtonen, 2005, Differential expression of IFN regulatory factor 4 gene in human monocyte-derived dendritic cells and macrophages, J. Immunol., 175, 6570, 10.4049/jimmunol.175.10.6570 · DOI
  117. Li, 2016, Somatosensory neuron types identified by high-coverage single-cell RNA-sequencing and functional heterogeneity, Cell Res., 26, 83, 10.1038/cr.2015.149 · DOI
  118. Li, 2015, Proinflammatory GM-CSF-producing B cells in multiple sclerosis and B cell depletion therapy, Sci. Transl. Med., 7, 10.1126/scitranslmed.aab4176 · DOI
  119. Liu, 2015, Notch signaling mediates granulocyte-macrophage colony-stimulating factor priming-induced transendothelial migration of human eosinophils, Allergy., 70, 805, 10.1111/all.12624 · DOI
  120. Liu, 2019, Role of GM-CSF in a mouse model of experimental autoimmune prostatitis, Am. J. Physiol. Renal Physiol., 317, F23, 10.1152/ajprenal.00013.2018 · DOI
  121. Llop-Guevara, 2014, A GM-CSF/IL-33 pathway facilitates allergic airway responses to sub-threshold house dust mite exposure, PLoS One., 9, 10.1371/journal.pone.0088714 · DOI
  122. Louis, 2015, Specific Contributions of CSF-1 and GM-CSF to the Dynamics of the Mononuclear Phagocyte System, J. Immunol., 195, 134, 10.4049/jimmunol.1500369 · DOI
  123. Magri, 2014, Innate lymphoid cells integrate stromal and immunological signals to enhance antibody production by splenic marginal zone B cells, Nat. Immunol., 15, 354, 10.1038/ni.2830 · DOI
  124. McQualter, 2001, Granulocyte macrophage colony-stimulating factor: a new putative therapeutic target in multiple sclerosis, J. Exp. Med., 194, 873, 10.1084/jem.194.7.873 · DOI · Paper page
  125. Metcalf, 1995, The hemopoietic colony-stimulating factors: from biology to clinical applications., 10.1017/CBO9780511663376 · DOI
  126. Molfino, 2016, Phase 2, randomised placebo-controlled trial to evaluate the efficacy and safety of an anti-GM-CSF antibody (KB003) in patients with inadequately controlled asthma, BMJ Open., 6, 10.1136/bmjopen-2015-007709 · DOI
  127. Murray, 2014, Macrophage activation and polarization: nomenclature and experimental guidelines, Immunity., 41, 14, 10.1016/j.immuni.2014.06.008 · DOI · Paper page
  128. Na, 2016, GM-CSF Grown Bone Marrow Derived Cells Are Composed of Phenotypically Different Dendritic Cells and Macrophages, Mol. Cells., 39, 734, 10.1016/molcells.2016.0160 · DOI
  129. Negishi, 2005, Negative regulation of Toll-like-receptor signaling by IRF-4, Proc. Natl. Acad. Sci. USA., 102, 15989, 10.1073/pnas.0508327102 · DOI
  130. Nicol, 2018, Central inhibition of granulocyte-macrophage colony-stimulating factor is analgesic in experimental neuropathic pain, Pain., 159, 550, 10.1097/j.pain.0000000000001130 · DOI
  131. Nieto, 2018, The Activin A-Peroxisome Proliferator-Activated Receptor Gamma Axis Contributes to the Transcriptome of GM-CSF-Conditioned Human Macrophages, Front. Immunol., 9, 31, 10.3389/fimmu.2018.00031 · DOI
  132. Nobs, 2019, GM-CSF intrinsically controls eosinophil accumulation in the setting of allergic airway inflammation, J. Allergy Clin. Immunol., 143, 1513, 10.1016/j.jaci.2018.08.044 · DOI
  133. Noguchi, 2001, Increased secretion of granulocyte-macrophage colony-stimulating factor in mucosal lesions of inflammatory bowel disease, Digestion., 63, 32, 10.1159/000051908 · DOI
  134. Noster, 2014, IL-17 and GM-CSF expression are antagonistically regulated by human T helper cells, Sci. Transl. Med., 6, 10.1126/scitranslmed.3008706 · DOI
  135. Oh, 2001, Chemokines and glycoprotein120 produce pain hypersensitivity by directly exciting primary nociceptive neurons, J. Neurosci., 21, 5027, 10.1523/JNEUROSCI.21-14-05027.2001 · DOI
  136. Papp, 2019, Granulocyte-macrophage colony-stimulating factor (GM-CSF) as a therapeutic target in psoriasis: randomized, controlled investigation using namilumab, a specific human anti-GM-CSF monoclonal antibody, Br. J. Dermatol., 180, 1352, 10.1111/bjd.17195 · DOI
  137. Pearson, 2016, ILC3 GM-CSF production and mobilisation orchestrate acute intestinal inflammation, eLife., 5, 10.7554/eLife.10066 · DOI
  138. Perugini, 2010, Alternative modes of GM-CSF receptor activation revealed using activated mutants of the common beta-subunit, Blood., 115, 3346, 10.1182/blood-2009-08-235846 · DOI
  139. Piccoli, 2015, Neutralization and clearance of GM-CSF by autoantibodies in pulmonary alveolar proteinosis, Nat. Commun., 6, 7375, 10.1038/ncomms8375 · DOI
  140. Ponomarev, 2007, GM-CSF production by autoreactive T cells is required for the activation of microglial cells and the onset of experimental autoimmune encephalomyelitis, J. Immunol., 178, 39, 10.4049/jimmunol.178.1.39 · DOI
  141. Puzanov, 2016, Talimogene Laherparepvec in Combination With Ipilimumab in Previously Untreated, Unresectable Stage IIIB-IV Melanoma, J. Clin. Oncol., 34, 2619, 10.1200/JCO.2016.67.1529 · DOI
  142. Rasouli, 2015, Expression of GM-CSF in T Cells Is Increased in Multiple Sclerosis and Suppressed by IFN-β Therapy, J. Immunol., 194, 5085, 10.4049/jimmunol.1403243 · DOI
  143. Rauch, 2012, Innate response activator B cells protect against microbial sepsis, Science., 335, 597, 10.1126/science.1215173 · DOI
  144. Reynolds, 2016, Synovial CD4+ T-cell-derived GM-CSF supports the differentiation of an inflammatory dendritic cell population in rheumatoid arthritis, Ann. Rheum. Dis., 75, 899, 10.1136/annrheumdis-2014-206578 · DOI
  145. Ribechini, 2017, Novel GM-CSF signals via IFN-γR/IRF-1 and AKT/mTOR license monocytes for suppressor function, Blood Adv., 1, 947, 10.1182/bloodadvances.2017006858 · DOI
  146. Ridwan, 2012, Distribution of granulocyte-monocyte colony-stimulating factor and its receptor α-subunit in the adult human brain with specific reference to Alzheimer’s disease, J. Neural Transm. (Vienna)., 119, 1389, 10.1007/s00702-012-0794-y · DOI
  147. Rogers, 2017, Analysis of the developmental stages, kinetics, and phenotypes exhibited by myeloid cells driven by GM-CSF in vitro, PLoS One., 12, 10.1371/journal.pone.0181985 · DOI
  148. Roth, 2012, Sargramostim (GM-CSF) for induction of remission in Crohn’s disease: a cochrane inflammatory bowel disease and functional bowel disorders systematic review of randomized trials, Inflamm. Bowel Dis., 18, 1333, 10.1002/ibd.22973 · DOI
  149. Sallese, 2017, Targeting cholesterol homeostasis in lung diseases, Sci. Rep., 7, 10211, 10.1038/s41598-017-10879-w · DOI
  150. Samavedam, 2014, GM-CSF modulates autoantibody production and skin blistering in experimental epidermolysis bullosa acquisita, J. Immunol., 192, 559, 10.4049/jimmunol.1301556 · DOI
  151. Schäbitz, 2008, A neuroprotective function for the hematopoietic protein granulocyte-macrophage colony stimulating factor (GM-CSF), J. Cereb. Blood Flow Metab., 28, 29, 10.1038/sj.jcbfm.9600496 · DOI
  152. Schneider, 2014, Induction of the nuclear receptor PPAR-γ by the cytokine GM-CSF is critical for the differentiation of fetal monocytes into alveolar macrophages, Nat. Immunol., 15, 1026, 10.1038/ni.3005 · DOI
  153. Scholz, 2017, GM-CSF in murine psoriasiform dermatitis: Redundant and pathogenic roles uncovered by antibody-induced neutralization and genetic deficiency, PLoS One., 12, 10.1371/journal.pone.0182646 · DOI
  154. Schön, 2000, Critical role of neutrophils for the generation of psoriasiform skin lesions in flaky skin mice, J. Invest. Dermatol., 114, 976, 10.1046/j.1523-1747.2000.00953.x · DOI
  155. Schweizerhof, 2009, Hematopoietic colony-stimulating factors mediate tumor-nerve interactions and bone cancer pain, Nat. Med., 15, 802, 10.1038/nm.1976 · DOI
  156. Shaposhnik, 2007, Granulocyte macrophage colony-stimulating factor regulates dendritic cell content of atherosclerotic lesions, Arterioscler. Thromb. Vasc. Biol., 27, 621, 10.1161/01.ATV.0000254673.55431.e6 · DOI
  157. Sheih, 2017, GM-CSF produced by the airway epithelium is required for sensitization to cockroach allergen, Mucosal Immunol., 10, 705, 10.1038/mi.2016.90 · DOI
  158. Sheng, 2014, STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation, Cell Res., 24, 1387, 10.1038/cr.2014.154 · DOI · Paper page
  159. Shiomi, 2014, GM-CSF but not IL-17 is critical for the development of severe interstitial lung disease in SKG mice, J. Immunol., 193, 849, 10.4049/jimmunol.1303255 · DOI
  160. Sonderegger, 2008, GM-CSF mediates autoimmunity by enhancing IL-6-dependent Th17 cell development and survival, J. Exp. Med., 205, 2281, 10.1084/jem.20071119 · DOI
  161. Song, 2015, Unique and redundant functions of NKp46+ ILC3s in models of intestinal inflammation, J. Exp. Med., 212, 1869, 10.1084/jem.20151403 · DOI
  162. Spath, 2017, Dysregulation of the Cytokine GM-CSF Induces Spontaneous Phagocyte Invasion and Immunopathology in the Central Nervous System, Immunity., 46, 245, 10.1016/j.immuni.2017.01.007 · DOI
  163. Stanley, 1994, Granulocyte/macrophage colony-stimulating factor-deficient mice show no major perturbation of hematopoiesis but develop a characteristic pulmonary pathology, Proc. Natl. Acad. Sci. USA., 91, 5592, 10.1073/pnas.91.12.5592 · DOI
  164. Sterner, 2019, GM-CSF inhibition reduces cytokine release syndrome and neuroinflammation but enhances CAR-T cell function in xenografts, Blood., 133, 697, 10.1182/blood-2018-10-881722 · DOI
  165. Stock, 2016, GM-CSF primes cardiac inflammation in a mouse model of Kawasaki disease, J. Exp. Med., 213, 1983, 10.1084/jem.20151853 · DOI
  166. Stösser, 2011, Hematopoietic colony-stimulating factors: new players in tumor-nerve interactions, J. Mol. Med. (Berl.)., 89, 321, 10.1007/s00109-010-0697-z · DOI
  167. Su, 2014, A positive feedback loop between mesenchymal-like cancer cells and macrophages is essential to breast cancer metastasis, Cancer Cell., 25, 605, 10.1016/j.ccr.2014.03.021 · DOI
  168. Sun, 2018, GM-CSF quantity has a selective effect on granulocytic vs. monocytic myeloid development and function, Front. Immunol., 9, 1922, 10.3389/fimmu.2018.01922 · DOI
  169. Suzuki, 2004, Activities of granulocyte-macrophage colony-stimulating factor and interleukin-3 on monocytes, Am. J. Hematol., 75, 179, 10.1002/ajh.20010 · DOI
  170. Suzuki, 2004, Critical roles of interferon regulatory factor 4 in CD11bhighCD8alpha- dendritic cell development, Proc. Natl. Acad. Sci. USA., 101, 8981, 10.1073/pnas.0402139101 · DOI
  171. Takeuchi, 2015, Efficacy and safety of mavrilimumab in Japanese subjects with rheumatoid arthritis: findings from a Phase IIa study, Mod. Rheumatol., 25, 21, 10.3109/14397595.2014.896448 · DOI
  172. Taylor, 2019, Efficacy and safety of namilumab, a human monoclonal antibody against granulocyte-macrophage colony-stimulating factor (GM-CSF) ligand in patients with rheumatoid arthritis (RA) with either an inadequate response to background methotrexate therapy or an inadequate response or intolerance to an anti-TNF (tumour necrosis factor) biologic therapy: a randomized, controlled trial, Arthritis Res. Ther., 21, 101, 10.1186/s13075-019-1879-x · DOI
  173. Thakur, 2014, Defining the nociceptor transcriptome, Front. Mol. Neurosci., 7, 87, 10.3389/fnmol.2014.00087 · DOI
  174. Timoshanko, 2005, Granulocyte macrophage colony-stimulating factor expression by both renal parenchymal and immune cells mediates murine crescentic glomerulonephritis, J. Am. Soc. Nephrol., 16, 2646, 10.1681/ASN.2004121107 · DOI
  175. Trapnell, 2019, Pulmonary alveolar proteinosis, Nat. Rev. Dis. Primers., 5, 16, 10.1038/s41572-019-0066-3 · DOI
  176. Tugues, 2018, Graft-versus-host disease, but not graft-versus-leukemia immunity, is mediated by GM-CSF-licensed myeloid cells, Sci. Transl. Med., 10, 10.1126/scitranslmed.aat8410 · DOI
  177. Uchida, 2009, Granulocyte/macrophage-colony-stimulating factor autoantibodies and myeloid cell immune functions in healthy subjects, Blood., 113, 2547, 10.1182/blood-2008-05-155689 · DOI
  178. van de Laar, 2012, Regulation of dendritic cell development by GM-CSF: molecular control and implications for immune homeostasis and therapy, Blood., 119, 3383, 10.1182/blood-2011-11-370130 · DOI
  179. Van der Borght, 2018, Myocarditis Elicits Dendritic Cell and Monocyte Infiltration in the Heart and Self-Antigen Presentation by Conventional Type 2 Dendritic Cells, Front. Immunol., 9, 2714, 10.3389/fimmu.2018.02714 · DOI
  180. van Nieuwenhuijze, 2014, Transgenic expression of GM-CSF in T cells causes disseminated histiocytosis, Am. J. Pathol., 184, 184, 10.1016/j.ajpath.2013.09.014 · DOI
  181. van Nieuwenhuijze, 2015, Complementary action of granulocyte macrophage colony-stimulating factor and interleukin-17A induces interleukin-23, receptor activator of nuclear factor-κB ligand, and matrix metalloproteinases and drives bone and cartilage pathology in experimental arthritis: rationale for combination therapy in rheumatoid arthritis, Arthritis Res. Ther., 17, 163, 10.1186/s13075-015-0683-5 · DOI
  182. Vlahos, 2006, Therapeutic potential of treating chronic obstructive pulmonary disease (COPD) by neutralising granulocyte macrophage-colony stimulating factor (GM-CSF), Pharmacol. Ther., 112, 106, 10.1016/j.pharmthera.2006.03.007 · DOI
  183. Wang, 2014, Interleukin-3/granulocyte macrophage colony-stimulating factor receptor promotes stem cell expansion, monocytosis, and atheroma macrophage burden in mice with hematopoietic ApoE deficiency, Arterioscler. Thromb. Vasc. Biol., 34, 976, 10.1161/ATVBAHA.113.303097 · DOI
  184. Wang, 2013, Characterization of pathogenic human monoclonal autoantibodies against GM-CSF, Proc. Natl. Acad. Sci. USA., 110, 7832, 10.1073/pnas.1216011110 · DOI
  185. Weber, 2011, CCL17-expressing dendritic cells drive atherosclerosis by restraining regulatory T cell homeostasis in mice, J. Clin. Invest., 121, 2898, 10.1172/JCI44925 · DOI
  186. Weber, 2014, Pleural innate response activator B cells protect against pneumonia via a GM-CSF-IgM axis, J. Exp. Med., 211, 1243, 10.1084/jem.20131471 · DOI
  187. Weinblatt, 2018, A Randomized Phase IIb Study of Mavrilimumab and Golimumab in Rheumatoid Arthritis, Arthritis Rheumatol., 70, 49, 10.1002/art.40323 · DOI
  188. Wicks, 2016, Targeting GM-CSF in inflammatory diseases, Nat. Rev. Rheumatol., 12, 37, 10.1038/nrrheum.2015.161 · DOI
  189. Willart, 2012, Interleukin-1α controls allergic sensitization to inhaled house dust mite via the epithelial release of GM-CSF and IL-33, J. Exp. Med., 209, 1505, 10.1084/jem.20112691 · DOI
  190. Willebrand, 2016, IL-33-Induced Cytokine Secretion and Survival of Mouse Eosinophils Is Promoted by Autocrine GM-CSF, PLoS One., 11, 10.1371/journal.pone.0163751 · DOI
  191. Williams, 2013, Transcription factor IRF4 drives dendritic cells to promote Th2 differentiation, Nat. Commun., 4, 2990, 10.1038/ncomms3990 · DOI
  192. Wright, 2013, RNA-seq reveals activation of both common and cytokine-specific pathways following neutrophil priming, PLoS One., 8, 10.1371/journal.pone.0058598 · DOI
  193. Wu, 2016, Pathogenic IL-23 signaling is required to initiate GM-CSF-driven autoimmune myocarditis in mice, Eur. J. Immunol., 46, 582, 10.1002/eji.201545924 · DOI
  194. Xu, 2008, The role of granulocyte macrophage-colony-stimulating factor in acute intestinal inflammation, Cell Res., 18, 1220, 10.1038/cr.2008.310 · DOI
  195. Yamada, 2017, Th1 is the predominant helper T cell subset that produces GM-CSF in the joint of rheumatoid arthritis, RMD Open., 3, 10.1136/rmdopen-2017-000487 · DOI
  196. Yamashita, 2002, Attenuation of airway hyperresponsiveness in a murine asthma model by neutralization of granulocyte-macrophage colony-stimulating factor (GM-CSF), Cell. Immunol., 219, 92, 10.1016/S0008-8749(02)00565-8 · DOI
  197. Yang, 2001, Dependence of interleukin-1-induced arthritis on granulocyte-macrophage colony-stimulating factor, Arthritis Rheum., 44, 111, 10.1002/1529-0131(200101)44:1<111::AID-ANR15>3.0.CO;2-1 · DOI
  198. Yashiro, 2018, The Transcription Factors PU.1 and IRF4 Determine Dendritic Cell-Specific Expression of RALDH2, J. Immunol., 201, 3677, 10.4049/jimmunol.1800492 · DOI
  199. Ye, 2013, GM-CSF contributes to aortic aneurysms resulting from SMAD3 deficiency, J. Clin. Invest., 123, 2317, 10.1172/JCI67356 · DOI
  200. Yong, 1992, Granulocyte-macrophage colony-stimulating factor induces neutrophil adhesion to pulmonary vascular endothelium in vivo: role of beta 2 integrins, Blood., 80, 1565, 10.1182/blood.V80.6.1565.1565 · DOI

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Metadata

Authors
Hamilton, J. A.
Affiliations
The University of Melbourne, Department of Medicine, Royal Melbourne Hospital, Parkville, Victoria, Australia 1
ORCID
Hamilton, John A.
Venue
Journal of Experimental Medicine
Publisher
Rockefeller University Press
Published
2019-10-14
Volume
217
Issue
1
ISSN
  • 0022-1007
  • 1540-9538
DOI
10.1084/jem.20190945
PMC
PMC7037240
Cited by
301
References
12
Language
en
Licence
Funders
National Health and Medical Research Council (1085240)

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