BACKGROUND: Coronavirus 2 (SARS-CoV-2), which causes severe acute respiratory syndrome in COVID-19, leads to complex immune reactions, hyperactivation of immunocompetent cells, including increased degranulation activity of mast cells and the release of their secretome products. The SARS-CoV-2 virus and the subsequent strong immune and inflammatory response, as well as a violation of the regulation of coagulation and fibrinolytic pathways, cause massive activation of latent TGF-β in the lungs, as well as the latent pool of TGF-β in the blood of patients with COVID-19. AIMS: To assume the participation of transforming growth factor-β (TGF-β) in lung damage in patients with COVID-19 by determining its quantitative level in autopsy lung samples in patients with COVID-19 and to conduct a correlation analysis with clinical and laboratory parameters. MATERIALS AND METHODS: The study included samples of lung autopsy material obtained from patients who died from severe COVID-19. A correlation analysis of TGF-β-positive cells and clinical and laboratory parameters was also performed. RESULTS: Extensive representation of TGF-β-positive cells was found in lung tissues of patients who died from COVID-19.A negative correlation was revealed: between TGF-β and the content of nucleated neutrophils in the blood (r = - 0,617; p = 0,033); between TGF-β and the level of C-reactive protein (CRP) according to the results of blood biochemistry (r = - 0,491; p = 0,013). A positive correlation was revealed between TGF-β and the content of blood platelets (r = 0,384; p =0,012);TGF-β with the level of erythrocyte sedimentation rate (ESR) (r = 0,409; p = 0,025). A positive correlation was also found between TGF-β and the presence of cough in the patient at the beginning of hospitalization (r = 0,367; p = 0,046). CONCLUSIONS: Activation of TGF-β in the lungs of patients who died from severe COVID-19 correlates with the level of neutrophils, platelets, ESR, CRP and the presence of cough in the patient. Further research is needed on the activation, release of TGF-β and its interactions in larger cohorts of patients. These correlations suggest the negative involvement of the transforming growth factor and consider the therapeutic possibilities of regulatory influence on its activation.