Distribution of γδ T cells in patients with hematological malignancies

Tumor progression in multiple myeloma (MM) is due to intrinsic features of myeloma cells and to interactions of myeloma cells with the bone marrow microenvironment. Beside promoting myeloma cell survival and proliferation, these interactions are responsible for: 1) the activation and differentiation of osteoclast precursors into mature osteoclasts, yielding to bone resorption and lytic lesions, 2) the angiogenic switch sustained by endothelial cells and other stromal cells, via paracrine and autocrine loops, involving multiple VEGF/VEGF-R and other pathways; 3) a progressive immune failure that is responsible for the enhanced susceptibility to infections of MM patients and the escape of myeloma cells to host immune surveillance.