Abstract
This review is dedicated to the mechanisms of antitumor immunity and to the features of its formation.
Immune checkpoint inhibitors have changed the treatment paradigm for cancer patients. Immunotherapy has shown superior efficacy to standard chemotherapy in many malignant neoplasms. This paper reviews literature data on the mechanisms of specific anti-tumour immunity and resistance of malignant neoplasms (MN) to immune checkpoint inhibitors. The following markers are widely used to determine the efficacy of checkpoint inhibitors in clinical practice PD-L1 status and microsatellite instability. Research shows that the level of PD-L1 expression determines the effectiveness of immunotherapy. The presence of high microsatellite instability determines sensitivity to ICT therapy regardless of histological subtype. The presence of PD-L1 and MSI status is an indication for the prescription of PD1 and PD-L1 immune checkpoint blockers. Even in the presence of MSI and high expression of PD-L1, a certain group of patients do not respond to therapy, indicating resistance and a lack of specific antitumor immunity. V(D)J DNA recombinations ensure the production of different antigen receptors in developing T and B lymphocytes, which appears to be a key factor in the development of specific antitumor immunity. TREC and KREC metrics should be considered to determine the efficacy of immunotherapy.
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