The
granulocyte colony-stimulating factor (
G-CSF), now referred to as CSF3, is a very important cell
growth factor that supports the proliferation, survival, and differentiation of neutrophilic progenitor cells, and also is a strong immune regulator of T cells and a promising therapeutic tool in acute
graft versus host disease (GVHD).
G-CSF acts by binding to its receptor G-CSFR (also called CSF3R), a member of the
cytokine receptor type I superfamily, which after binding with
G-CSF activates the canonical
Janus kinase (Jak)/signal transducer, activator of transcription (STAT)and Ras/Raf/MAP
kinase pathways.
G-CSF has been applied to the clinic to treat congenital and acquired
neutropenia before or during courses of intensive
chemotherapy. It has also been applied to mobilize hematopoietic stem cells into the peripheral blood for Auto-or
allogeneic transplantation, and the priming strategies designed to enhance the sensitivity of
leukemia stem cells to
cytotoxic agents in protocols aimed to induce their differentiation, accompanying growth arrest, and cell death. With the rapid development of molecular genetics and clinical research, CSF3R mutations have been implicated in the progression of
severe congenital neutropenia (SCN) to
leukemia. Recently, CSF3R mutations have been discovered frequently in
chronic neutrophilic leukemia (CNL). Such findings might provide the theoretical basis for the targeted
therapy. In this review, the clinical application of
G-CSF receptor in hematonosis is briefhy summarized.