When it comes to tumor immunology, understanding of molecular pathways is rather important. During oncogenesis, many molecules should be taken in consideration altogether in context of a single malignancy. It is of a great significance to determine whether these molecules act synergistically or contrary, whether to understand a malignant disease more thoroughly, or even more important, to reveal new approaches of therapy. In this review, we discuss whether and how IL-33/ST2 and PD-1/PDL axis involve in antitumor immunity.
Introduction: Immune checkpoint therapy is well- established therapeutic approach in treatment of malignant disease and is thought to be mostly based on facilitating adaptive immune responses. However, cells of innate immune response, such as NKT cells, might also be important for successful anti-programmed cell death protein 1 therapy, as they initiate anti-tumor immune response. Materials and methods: For tumor induction, 4T1 cells syngenic to BALB/c background were used after which mice underwent anti-programmed cell death protein 1 treatment.After the mice were sacrificed, NKT cells, dendritic cells and macrophages derived from spleen and primary tumor tissue were analyzed using flow cytometry. Results: Anti-programmed cell death protein 1 therapy significantly decelerates tumor growth and enhanced expression of activating molecules CD69, NKp46, NKG2D in NKT cells of tumor and spleen. Anti-programmed cell death protein 1 therapy activates pro-tumoricidic changes in dendritic cells and macrophages of primary tumor tissue. Conclusion: Anti-programmed cell death protein 1 therapy activates NKT cell directly, and indirectly via DCs. Activated NKT cells provide tumoricidic properties directly, by secreting perforin, and indirectly by stimulating M1 macrophages polarization. Since anti-programmed cell death protein 1 therapy induces significant changes in NKT cells, dendritic cells and macrophages, efficacy of overall anti-programmed cell death protein 1 therapy is increased, contributing to more efficient anti-tumor immune response.
Background A new virus from the group of coronaviruses was identified as the cause of atypical pneumonia and called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and disease called Corona Virus Disease (COVID-19). During the cytokine storm, the main cause of the death, proinflammatory cytokines are released which stimulate further tissue destruction. Galectin-1 is pleiotropic cytokine involved in many immune and inflammatory processes and its role in COVID-19 is still unknown. Objective The aim of this study was to determine systemic values of galectin-1 and correlations between gal-1 and proinflammatory cytokines and clinical parameters during COVID-19 progression. Design Observational and cross-sectional study. Patients 210 COVID-19 patients were included and divided into mild, severe or critical group according to COVID-19 severity. Main Measures Serum levels of IL-1β, IL-6, IL-10, IL-23, IL-33 and galectin-1 were measured using sensitive enzyme-linked immunosorbent assay (ELISA) kits. Key Results Systemic levels of IL-1β, IL-6, IL-10, IL-23, IL-33 and galectin-1 were significantly higher in stage III of COVID-19 patients compared to stage I and II. There were no significant differences in ratio between Galectin-1 and IL-10 with proinflammatory cytokines. Positive correlation was detected between Gal-1 and IL-1β, IL6, IL-10, IL-23 and IL-33. Gal-1 positively correlated with chest radiographic finding, dry cough and headache and negatively correlated with normal breathing sound. Conclusions Linear regression model and ROC curve analysis point on Gal-1 as significant predictors for COVID-19 severity. Presented results implicate on Gal-1 and IL-10 dependent immunomodulation. The precise mechanism of Gal-1 effect in COVID-19 and its potential as a stage marker of disease severity is still to be clarified.
Galectin-3 (Gal-3), multifunctional protein plays important roles in inflammatory response, infection and fibrosis. The goal of study was to determine the association of Gal-3, immune response, clinical, biochemical, and radiographic findings with COVID-19 severity. Study included 280 COVID-19 patients classified according to disease severity into mild, moderate, severe and critical group. Cytokines, clinical, biochemical, radiographic data and peripheral blood immune cell make up were analyzed. Patients in critical group had significantly higher serum level of Gal-3, IL-1β, TNF-α, IL-12, IL-10 compared to the patients in less severe stages of disease. Strong positive correlation was detected between Gal-3 and IL-1β, moderate positive correlation between Gal-3, TNF-α and IL-12, moderate negative correlation between Gal-3, IL-10/IL-1β and IL-10/TNF-α. Moderate positive correlation noted between Gal-3 and urea, D dimer, CXR findings. Strong negative correlation detected between Gal-3 and p02, Sa02, and moderate negative correlation between Gal-3, lymphocyte and monocyte percentage. In the peripheral blood of patients with more severe stages of COVID-19 we detected significantly increased percentages of CD56− CD3+TNF-α+T cells and CD56− CD3+Gal-3+T cells and increased expression of CCR5 in PBMCs. Our results predict Gal-3 as an important marker for critical stage of COVID-19. Higher expression of Gal-3, TNF-α and CCR5 on T cells implicate on promoting inflammation and more severe form of disease.
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