Recombinant G-CSF Treatment of Severe Chronic Neutropenia in Neonates and Infants

Christensen, Robert D.

doi:10.1007/978-3-319-18159-2_245-1

Cited by 1 publication

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“…In the therapeutic setting, major applications of administration of recombinant (r) G-CSF include: (i) attenuation of the magnitude and duration of chemotherapy-induced neutropenia in cancer patients [ 2 ], described in greater detail below; (ii) treatment of cyclic and chronic neutropenias [ 3 , 4 ]; and (iii) mobilization of hematopoietic progenitor cells into peripheral blood to be harvested for stem cell transplantation. In the latter setting, the incidence and severity of experimental acute graft-versus-host disease (aGVHD) are also reduced by administration of rG-CSF [ 5 , 6 ], seemingly due to the immunoregulatory effects of rG-CSF on cells of both the innate and adaptive immune systems, especially T cells, as reviewed earlier by Yang et al [ 7 ], as well as immature neutrophils [ 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

Contrasting Immunopathogenic and Therapeutic Roles of Granulocyte Colony-Stimulating Factor in Cancer

2020

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Tumor cells are particularly adept at exploiting the immunosuppressive potential of neutrophils as a strategy to achieve uncontrolled proliferation and spread. Recruitment of neutrophils, particularly those of an immature phenotype, known as granulocytic myeloid-derived suppressor cells, is achieved via the production of tumor-derived granulocyte colony-stimulating factor (G-CSF) and neutrophil-selective chemokines. This is not the only mechanism by which G-CSF contributes to tumor-mediated immunosuppression. In this context, the G-CSF receptor is expressed on various cells of the adaptive and innate immune systems and is associated with induction of T cell polarization towards the Th2 and regulatory T cell (Treg) phenotypes. In contrast to the potentially adverse effects of sustained, endogenous production of G-CSF by tumor cells, stringently controlled prophylactic administration of recombinant (r) G-CSF is now a widely practiced strategy in medical oncology to prevent, and in some cases treat, chemotherapy-induced severe neutropenia. Following an overview of the synthesis, structure and function of G-CSF and its receptor, the remainder of this review is focused on: (i) effects of G-CSF on the cells of the adaptive and innate immune systems; (ii) mechanisms by which this cytokine promotes tumor progression and invasion; and (iii) current clinical applications and potential risks of the use of rG-CSF in medical oncology.

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