Abstract
Haematological and non-haematological malignancies are able to escape the host immune by the capacity to hijack the immune check-points [...]
Highlights
Haematological and non-haematological malignancies are able to escape the host immune by the capacity to hijack the immune check-points
The resulting inflammation leads to the expression of PD-L1 by hematopoietic, epithelial and endothelial cells, activating programmed death-1 (PD-1) on the surface of T-cells and blocking the immune response
Previous studies have found out that PD-1 is highly expressed on T-reg cells and their binding with PD-L1 enhances suppressor T-reg functions[2,3]; the activation of PD-1/PD-L1 pathway reduces the lytic capacity of NK cells and B cell antibody production
Summary
Haematological and non-haematological malignancies are able to escape the host immune by the capacity to hijack the immune check-points. Previous studies have found out that PD-1 is highly expressed on T-reg cells and their binding with PD-L1 enhances suppressor T-reg functions[2,3]; the activation of PD-1/PD-L1 pathway reduces the lytic capacity of NK cells and B cell antibody production. In solid neoplasms PD-L1 expression by cancer cells and persistent up-regulation of PD-1 by tumourinfiltrating lymphocytes is common[45]. All these findings brought to the development of check-point inhibitors in the contest of solid tumors and lymphoproliferative neoplasms such as lymphoma and myeloma where the immune checkpoint blockade treatment have shown efficacy in refractory/relapsed neoplasms[6]. To assess the presence of PD-1 and PD-L1 positive cells, by immunohistochemistry, in bone marrow biopsies of patients with AML
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