Figure 3.

Potential roles of basophils in the bone marrow (BM) of patients with CML. Chronic myeloid leukaemia (CML) is characterized by an increase and mobilization of clonal stem cells, extramedullary myelopoiesis and clonal basophilia. In addition, BM fibrosis and increased angiogenesis are typically found in CML. Basophils are known to produce and secrete several key mediators contributing to the pathogenesis and evolution of CML. These cells also increase in number during disease acceleration. Basophil‐derived dipeptidyl‐peptidase IV (DPPIV = CD26) cleaves stroma cell‐derived factor‐1 (SDF‐1) and thereby facilitates the mobilization of leukaemic stem cells (LSC) out of the niche. Basophil‐derived histamine and vascular endothelial growth factor (VEGF), also known as vascular permeability factor (VPF), can promote the transmigration of CML LSC and may facilitate the redistribution of these cells into the peripheral blood (PB) and may thereby trigger extramedullary myelopoiesis. Basophil‐derived hepatocyte growth factor (HGF) and basophil‐derived interleukins (ILs) may be involved in the regulation of growth and differentiation of CML LSC. Finally, basophil‐derived HGF, VEGF, angiopoietin‐1 (Ang‐1) and tryptase can induce the growth and accumulation of fibroblasts and endothelial cells and thereby can promote angiogenesis and fibrosis in the BM in CML