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Functional features of neutrophils induced by G-CSF and GM-CSF treatment: differential effects and clinical implications

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TLDR
This review summarizes major functional and phenotypical features of neutrophils induced by G-CSF treatment in patients with acquired and congenital neutropenias and focuses on the differential effect of G- CSF and GM-SF on neutrophil function in vitro and in vivo.
Abstract
G-CSF and GM-CSF are hematopoietic growth factors required for proliferation and differentiation of hematopoietic precursors. G-CSF is now widely used to overcome neutropenias of various origins. Beside the absolute number, the functional capacity of neutrophils at sites of inflammation is of major importance in host defense. This review summarizes major functional and phenotypical features of neutrophils induced by G-CSF treatment in patients with acquired and congenital neutropenias. Furthermore, we focus on the differential effect of G-CSF and GM-CSF on neutrophil function in vitro and in vivo. Some of the altered abilities of cytokine-induced neutrophils are important to understand side-effects of G-CSF therapy.

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Journal ArticleDOI

Lineage-specific hematopoietic growth factors.

TL;DR: This review surveys the mechanisms and clinical applications of three hematopoietic growth factors: erythropoietin, granulocyte colony-stimulating factor, and thrombopOietin.
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Tumour-associated neutrophils in patients with cancer

TL;DR: The evidence correlating the neutrophil-to-lymphocyte ratio with prognosis is described, followed by a discussion on the predictive value of TANs, which remains debatable, with conflicting data from different cancer types.
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Sweet's syndrome: a neutrophilic dermatosis classically associated with acute onset and fever.

TL;DR: Although a definitive mechanism of pathogenesis for the development of Sweet’s syndrome symptoms and lesions still remains to be determined, it is possible that cytokines—directly or indirectly—have an important role in the etiology of this condition.
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The Gene for Glycogen-Storage Disease Type 1b Maps to Chromosome 11q23

TL;DR: The linkage of the GSD-1b locus to genetic markers spanning a 3-cM region on chromosome 11q23 will provide new insights into the genetic bases of G6P metabolism and neutrophil-monocyte dysfunction.
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Sweet Syndrome: A Review and Update

TL;DR: In this article, a concise review of the pathogenesis, classification, diagnosis and treatment update of the sweet syndrome is presented, which is the most representative entity of febrile neutrophilic dermatoses.
References
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Journal ArticleDOI

Leukocyte-endothelial adhesion molecules.

TL;DR: Investigations have progressed from the early descriptions by intravital microscopy and histology, to functional and immunologic characterization of adhesion molecules, and now to the development of genetically deficient animals and the first phase I trial of "anti-adhesion" therapy in humans.
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Recombinant human granulocyte-macrophage colony-stimulating factor stimulates in vitro mature human neutrophil and eosinophil function, surface receptor expression, and survival.

TL;DR: It is shown that granulocyte-macrophage colony stimulating factor can selectively stimulate mature granulocytes function and induced morphological changes and enhanced the survival of both neutrophils and eosinophils by 6 and 9 h, respectively.
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Membrane Proteins Involved in Phagocyte Adherence to Endothelium

TL;DR: Le role d'antigenes tels que l'antigene cD18 dans l'emigration in vivo des phagocytes dans les mecanismes inflammatoires est etudie.
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Malignancy-associated Sweet's syndrome: review of the world literature.

TL;DR: All the manifestations of Sweet's syndrome improved dramatically with corticosteroid therapy, regardless of the response of the associated neoplasm to tumor-directed therapy.
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Sweet's syndrome and malignancy

TL;DR: The presence of anemia, abnormal platelet counts, immature cells in the differential, and/or severe vesiculobullous or ulcerative cutaneous lesions is infrequent in idiopathic Sweet's syndrome and should alert physicians to the possibility of a more serious underlying disease.
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