{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Schaunaman N"],"funding":["NIAID NIH HHS","National Institutes of Health","NIH HHS"],"pagination":["31"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8848971"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(1)"],"pubmed_abstract":["<h4>Background</h4>Toll-interacting protein (Tollip) is one of the key negative regulators in host innate immunity. Genetic variation of Tollip has been associated with less Tollip expression and poor lung function in asthmatic patients, but little is known about the role of Tollip in human airway type 2 inflammatory response, a prominent feature in allergic asthma.<h4>Objective</h4>Our goal was to determine the role and underlying mechanisms of Tollip in human airway epithelial responses such as eotaxin to type 2 cytokine IL-13.<h4>Methods</h4>Tollip deficient primary human airway epithelial cells from 4 healthy donors were generated by the gene knockdown approach and stimulated with IL-13 to measure activation of transcription factor STAT3, and eotaxin-3, an eosinophilic chemokine.<h4>Re"],"journal":["Respiratory research"],"pubmed_title":["Tollip interaction with STAT3: a novel mechanism to regulate human airway epithelial responses to type 2 cytokines."],"pmcid":["PMC8848971"],"funding_grant_id":["U19AI125357","R01 AI150082","U19 AI125357"],"pubmed_authors":["Schaunaman N","Kraft M","Chu HW","Dimasuay KG"],"additional_accession":[]},"is_claimable":false,"name":"Tollip interaction with STAT3: a novel mechanism to regulate human airway epithelial responses to type 2 cytokines.","description":"<h4>Background</h4>Toll-interacting protein (Tollip) is one of the key negative regulators in host innate immunity. Genetic variation of Tollip has been associated with less Tollip expression and poor lung function in asthmatic patients, but little is known about the role of Tollip in human airway type 2 inflammatory response, a prominent feature in allergic asthma.<h4>Objective</h4>Our goal was to determine the role and underlying mechanisms of Tollip in human airway epithelial responses such as eotaxin to type 2 cytokine IL-13.<h4>Methods</h4>Tollip deficient primary human airway epithelial cells from 4 healthy donors were generated by the gene knockdown approach and stimulated with IL-13 to measure activation of transcription factor STAT3, and eotaxin-3, an eosinophilic chemokine.<h4>Re","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2025-04-19T22:38:37.095Z","creation":"2025-04-19T22:38:37.095Z"},"accession":"S-EPMC8848971","cross_references":{"pubmed":["35172835"],"doi":["10.1186/s12931-022-01941-x"]}}