Cell Proliferation Induced by GM‑CSF and Neutralization by Mouse GM‑CSF Antibody. |
Recombinant Mouse GM‑CSF (Catalog # 415-ML) stimulates proliferation in the DA3 mouse myeloma cell line in a dose-dependent manner (orange line). Proliferation elicited by Recombinant Mouse GM‑CSF (0.1 ng/mL) is neutralized (green line) by increasing concentrations of Goat Anti-Mouse GM‑CSF Polyclonal Antibody (Catalog # AB-415-NA). The ND50 is typically 0.01‑0.05 µg/mL.
GM-CSF was initially characterized as a factor that can support the in vitro colony formation of granulocyte-macrophage progenitors. It is also a growth factor for erythroid, megakaryocyte, and eosinophil progenitors. GM-CSF is produced by a number of different cell types (including T cells, B cells, macrophages, mast cells, endothelial cells, fibroblasts, and adipocytes) in response to cytokine or inflammatory stimuli. On mature hematopoietic cells, GM-CSF is a survival factor for and activates the effector functions of granulocytes, monocytes/macrophages, and eosinophils. GM-CSF promotes a Th1 biased immune response, angiogenesis, allergic inflammation, and the development of autoimmunity. It shows clinical effectiveness in ameliorating chemotherapy-induced neutropenia, and GM-CSF transfected tumor cells are utilized as cancer vaccines. The 22 kDa glycosylated GM-CSF, similar to IL-3 and IL-5, is a cytokine with a core of four bundled alpha ‑helices. Mature mouse GM-CSF shares 49-54% amino acid sequence identity with canine, feline, human, and porcine GM-CSF and 69% with rat GM-CSF. GM‑CSF exerts its biological effects through a heterodimeric receptor complex composed of GM-CSF R alpha /CD116 and the signal transducing common beta chain (CD131) which is also a component of the high-affinity receptors for IL-3 and IL-5. In addition, GM-CSF binds a naturally occurring soluble form of GM-CSF R alpha. The activity of GM-CSF is species specific between human and mouse. Mouse GM-CSF is only weakly active on rat cells, although rat GM-CSF is fully active on mouse cells.
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