G-CSF ELISA Kit, Mouse

G-CSF stimulates the proliferation and differentiation of hematopoietic progenitor cells committed to the neutrophils and granulocytes lineage in a dose-dependent manner. At higher concentrations this factor induces the generation of colonies in soft agar cultures containing granulocytes and macrophages. The fully differentiated neutrophilic granulocytes are functionally activated by G-CSF. G-CSF is a mitogen for some human myeloid leukemia cells and also for some carcinoma cell lines. G-CSF synergises with some other cytokines, including GM-CSF and IL4. GM-CSF and G-CSF are required, for example, to develop neutrophilic colonies in vitro. The concerted action of G-CSF and Epo is required to support the growth of mixed colonies of the early erythroid progenitors.² A combination of IL4 with G-CSF has been shown to lead to synergistic suppression of the growth of some human leukemic cell lines.³

In vitro G-CSF enhances the antibody-dependent cell-mediated cytotoxicity of granulocytes against tumor cells. G-CSF induces the synthesis of receptors for fMLP (Formyl-Met-Leu-Phe) which, in turn, induces the prolonged production of oxygen radicals and the release of arachidonic acid. G-CSF also increases the synthesis of Fc-receptors for IgA. Unlike GM-CSF, G-CSF does not induce the expression of cellular markers such as CD11A and CD11C. The main and most important clinical application of G-CSF is probably the treatment of transient phases of leukopenia following chemotherapy and/or radiotherapy. G-CSF can be used to expand the myeloid cell lineage. It has been shown that the pretreatment with recombinant human G-CSF prior to marrow harvest can improve the graft by increasing the total number of myeloid lineage restricted progenitor cells, resulting in stable but not accelerated myeloid engraftment of autologous marrow.⁴