G-CSF is the key hematopoietic cytokine involved in the control of neutrophil development; therefore it is a critical regulator of innate immunity against bacterial infections. G-CSF mobilizes stem cells indirectly by down-regulating the expression of CXCL12 on marrow osteoblasts and by releasing neutrophil and monocyte proteolytic enzymes, including neutrophil elastase, cathepsin G, and matrix metalloproteinase-9, which in turn degrade important HSC-trafficking and adhesion molecules CD117 (c-kit), CD106 (VCAM-1), and CD184 (CXCR4). In addition, G-CSF possesses immunosuppressive effects on monocytes/macrophages, dendritic cells, and T lymphocytes. The receptor for G-CSF is expressed not only in hematopoietic cells; but also in cardiomyocytes, skeletal muscle, and neurons. G-CSF influences mouse skeletal muscle development and regeneration by stimulating myoblast proliferation. In vitro, G-CSF displays strong antiapoptotic activity in neuronal cells. Also, G-CSF has pleiotropic actions in the central nervous system. It has been reported to have neuroprotective effect in focal cerebral ischemia models and it counteracts programmed cell death and drives neurogenesis.