Abstract
Genetic and/or epigenetic changes provide antigen-derived diversity in neoplastic cells. Beside, these cells do not initiate immune response of host organisms. A variety of factors are responsible for the resistant to treatment, including individual variations in patients and somatic cell genetic differences in tumors, even those from the same tissue of origin. Immune system is controlled by several controlling mechanisms. Recently, a significant progress in hematologic treatment has been made; however, majority of diseases still remain incurable. Immunotherapy with checkpoint inhibitors has emerged as promising modality of antitumor treatment, showing marked response to several antigens, including cytotoxic T lymphocyte-associate protein-4 (CTLA-4) or programmed cell death 1 receptor (PD-1). In this review, we demonstrate actual knowledge on immune checkpoint function and its impact on development of new modality of antineoplastic treatment, using, for example, anti-CTLA-4 or PD-1/PD1 ligand (PD-L1) monoclonal antibodies in malignant lymphomas.