Tumor-induced myeloid deviation: when myeloid-derived suppressor cells meet tumor-associated macrophages

摘要: The generation of an inflammatory environment is favorable and often decisive for the growth both primary tumors metastases. Tumor cells either express membrane molecules or release tumor-derived soluble factors able to alter myelopoiesis. Tumor-reprogrammed myeloid not only create a tolerogenic by blocking T cell functions proliferation, but also directly drive tumor promoting cancer stemness, angiogenesis, stroma deposition, epithelial-to-mesenchymal transition, metastasis formation. In this Review, we discuss interplay between immunosuppressive protumoral detail their immune-regulatory mechanisms, molecular pathways involved in differentiation, as well potential role prognostic diagnostic biomarkers prospective targets innovative approaches treat tumor-bearing hosts.