G-CSF and GM-CSF in Neutropenia

Mehta, Hrishikesh; Malandra, Michael; Corey, Seth J.

doi:10.4049/jimmunol.1500861

Cited by 301 publications

(242 citation statements)

References 118 publications

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“…Numerous studies have shown that GM-CSF or G-CSF plays the central role in the regulation of cisplatin-induced granulocytopenia [11,12]. Mobilization of granulocytes and their progenitors from bone marrow to the blood stream is induced by GM-CSF or G-CSF [11,12].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Atrial natriuretic peptide protects against cisplatin-induced granulocytopenia

Nojiri

Hosoda

Zenitani

et al. 2016

Cancer Chemother Pharmacol

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Atrial natriuretic peptide protects against cisplatin-induced granulocytopenia

Nojiri

Hosoda

Zenitani

et al. 2016

Cancer Chemother Pharmacol

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“…G(M)-CSF signals through their each specific dimeric receptors to activate intracellular Janus kinase (JAK)/signal transducer and activator of transcription (STAT)/extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase signaling. 2 For many functions, G-CSF and GM-CSF can crosscover. For some functions, they cannot.…”

Section: Introductionmentioning

confidence: 99%

Glioblastoma-synthesized G-CSF and GM-CSF contribute to growth and immunosuppression: Potential therapeutic benefit from dapsone, fenofibrate, and ribavirin

Kast¹,

Hill

Wion

et al. 2017

Tumour Biol.

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Increased ratio of circulating neutrophils to lymphocytes is a common finding in glioblastoma and other cancers. Data reviewed establish that any damage to brain tissue tends to cause an increase in G-CSF and/or GM-CSF (G(M)-CSF) synthesized by the brain. Glioblastoma cells themselves also synthesize G(M)-CSF. G(M)-CSF synthesized by brain due to damage by a growing tumor and by the tumor itself stimulates bone marrow to shift hematopoiesis toward granulocytic lineages away from lymphocytic lineages. This shift is immunosuppressive and generates the relative lymphopenia characteristic of glioblastoma. Any trauma to brain-be it blunt, sharp, ischemic, infectious, cytotoxic, tumor encroachment, or radiation-increases brain synthesis of G(M)-CSF. G(M)-CSF are growth and motility enhancing factors for glioblastomas. High levels of G(M)-CSF contribute to the characteristic neutrophilia and lymphopenia of glioblastoma. Hematopoietic bone marrow becomes entrained with, directed by, and contributes to glioblastoma pathology. The antibiotic dapsone, the lipid-lowering agent fenofibrate, and the antiviral drug ribavirin are Food and Drug Administration-and European Medicines Agency-approved medicines that have potential to lower synthesis or effects of G(M)-CSF and thus deprive a glioblastoma of some of the growth promoting contributions of bone marrow and G(M)-CSF.

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“…Both G-CSF and GM-CSF are glycoproteins secreted from activated immune and endothelial cells sharing high sequence homology, both acting to promote the production, mobilization, and differentiation of hematopoietic stem cells. Both are used in recombinant form for the treatment of neutropenia and for mobilization of hematopoietic stem cells to the peripheral blood in transplantation [8]. CNS protective and recovery-promoting modulatory effects described for G-CSF on neurogenesis, angiogenesis, and immune activity in animal models of stroke, Alzheimer disease, and traumatic brain injury [9,10] have prompted its experimental use among stroke patients, with a lack of clear beneficial results to date [11].…”

Section: Discussionmentioning

confidence: 99%

Long-Term Immune Alterations Accompanying Chronic Posttraumatic Stress Disorder following Exposure to Suicide Bomb Terror Incidents during Childhood

et al. 2017

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Background and Aim: Long-term immune alterations have been proposed to play a mechanistic role in posttraumatic stress disorder (PTSD) as well as in its associated increase in medical morbidity and mortality. Better characterization of altered immune function may help identify diagnostic and prognostic biomarkers and potentially targets for preventive intervention. Methods: As part of an ongoing study, we conducted a preliminary case-control comparison of resting immune inflammatory profiles between terror victims treated in childhood at the emergency department over the previous decade, who developed chronic PTSD upon long-term follow-up, and healthy controls. Results: Our preliminary results in a subsample of this ongoing study support and extend elevated resting levels of granulocyte colony-stimulating factor, interleukin-4, and regulated on activation, normal T cell expressed and secreted in childhood onset chronic PTSD. Conclusion: Chronic immune alterations may participate in inflammatory activation and signal to the CNS through the neurovascular unit, as well as modulate the neuroendocrine axis. Better characterization and understanding of these preliminary findings may point to diagnostic and prognostic biomarkers and potentially elucidate mechanistic involvement of immune activation in PTSD.

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G-CSF and GM-CSF in Neutropenia

Cited by 301 publications

References 118 publications

RETRACTED ARTICLE: Atrial natriuretic peptide protects against cisplatin-induced granulocytopenia

RETRACTED ARTICLE: Atrial natriuretic peptide protects against cisplatin-induced granulocytopenia

Glioblastoma-synthesized G-CSF and GM-CSF contribute to growth and immunosuppression: Potential therapeutic benefit from dapsone, fenofibrate, and ribavirin

Long-Term Immune Alterations Accompanying Chronic Posttraumatic Stress Disorder following Exposure to Suicide Bomb Terror Incidents during Childhood

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