Abstract
Epithelial cell-derived cytokines such as TSLP (thymic stromal lymphopoietin), IL-25 and IL-33 initiate type 2 immune response via activation of type 2 innate lymphoid cells (ILC2). ILC2s, predominantly located in the lung are a novel cell population that produce Th2 cytokines. In vitro experiments showed that TSLP signaling in ILC2 cells augmented proinflammatory cytokine production. Knowledge of ILC2 cells comes mainly from in vitro experiments or animal model The aim of the study was to define the TSLP expression and its role in the activation of Th2 response in obstructive lung diseases Methods: the study enrolled 38 patients: 12 of IgE-mediated asthma, 16 with COPD and 10 controls who underwent lung function test and sputum induction. In induced sputum (IS) mRNA and protein expression levels of IL-4, IL-13, TSLP and tryptase were evaluated (by real-time PCR and ELISA method, respectively) Results: patients with asthma and COPD had elevated concentration of TSLP in IS vs. control. In the asthma group we reported significantly higher eosinophil percentage and elevated levels of all cytokines vs. control. In the COPD we noted a statistically higher percentage of neutrophils and elevated mRNA levels of all investigated cytokines vs. controls. We noticed a significant positive correlation between TSLP and IL-13 or IL-4 level. In all groups concentration of TSLP positively correlated with the percentage of neutrophils, and with the value of FEV1% and FEV 1 %VC Conclusions: TSLP expression is associated with activation of Th2 response what suggests the possible role of TSLP in the regulation of ILC2s. We believe that therapeutic strategies to target ILC2 via TSLP downregulation may be useful in afflicted individuals.
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