Granulocyte colony stimulating factor (G-CSF) is an essential cytokine frequently used in clinics to restore myelopoiesis and facilitate peripheral mobilization of hematopoietic stem cells. Endogenously secreted G-CSF acts as a pleiotropic growth factor and mediates its biological functions [granulopoiesis] by binding specifically to granulocyte colony stimulating factor receptor (G-CSF-R). The G-CSF-G-CSF-R pathway known for its pro-Th2 and anti- inflammatory properties has been successful in reversing the course of diseases such as type 1 diabetes (T1D) and myelin basic protein-induced experimental autoimmune encephalomyelitis (MOG-EAE). The promising benefits of G-CSF have helped in establishing it as a successful candidate for several clinical trials. Even though cytokine based immune intervention offers a highly feasible and attractive option for immune disease control, caution needs to exerted on its usage as the functions of most cytokines vary depending upon the disease where they are applied, the research model being tested, as well as the modality of treatment (e.g., dose, duration and route) and, G-CSF despite its beneficial anti- inflammatory properties has also exerted bifurcated roles depending upon the disorder and dosage in which it’s applied.
This review aims to summarize the findings associated with the function and role of granulocyte colony-stimulating factor (G-CSF) and its dichotomous role in immune related therapies. Here we specifically focus on SLE and T1D, two autoimmune disorders in which G-CSF may exert physiological effects in opposite directions.