{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["13"],"submitter":["Tomiaki C"],"pubmed_abstract":["Asthma is airway inflammatory diseases caused by the activation of group 2 innate lymphoid cells (ILC2s) and type 2 helper T (T<sub>H</sub>2) cells. Cysteine proteases allergen cause tissue damage to airway epithelial cells and activate ILC2-mediated type 2 airway inflammation. FK506 is an immunosuppressive agent against calcium-dependent NFAT activation that is also effective against asthmatic inflammation. However, the effects of FK506 on cysteine protease allergen-mediated airway inflammation remain unclear. In this study, we investigated the suppressive effects of FK506 on airway inflammation. FK506 had a partial inhibitory effect on ILC2-dependent eosinophil inflammation and a robust inhibitory effect on T cell-dependent eosinophil inflammation in a cysteine protease-induced mouse asthma model. The infiltration of T1/ST2<sup>+</sup> CD4 T cells in the lungs contributed to the persistence of eosinophil infiltration in the airway; FK506 completely inhibited the infiltration of T1/ST2<sup>+</sup> CD4 T cells. In the initial phase, FK506 treatment targeted lung ILC2 activation induced by leukotriene B<sub>4</sub> (LTB<sub>4</sub>)-mediated calcium signaling, but not IL-33 signaling. FK506 also inhibited the IL-13-dependent accumulation of T1/ST2<sup>+</sup> CD4 T cells in the lungs of the later responses. These results indicated that FK506 potently suppressed airway inflammation by targeting ILC2 activation and T1/ST2<sup>+</sup> CD4 T cell accumulation."],"journal":["Frontiers in immunology"],"pagination":["1014462"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9683035"],"repository":["biostudies-literature"],"pubmed_title":["Role of FK506-sensitive signals in asthmatic lung inflammation."],"pmcid":["PMC9683035"],"pubmed_authors":["Miyauchi K","Ki S","Mukoyama Y","Morimoto H","Suzuki N","Suzuki Y","Kubo M","Tomiaki C"],"additional_accession":[]},"is_claimable":false,"name":"Role of FK506-sensitive signals in asthmatic lung inflammation.","description":"Asthma is airway inflammatory diseases caused by the activation of group 2 innate lymphoid cells (ILC2s) and type 2 helper T (T<sub>H</sub>2) cells. Cysteine proteases allergen cause tissue damage to airway epithelial cells and activate ILC2-mediated type 2 airway inflammation. FK506 is an immunosuppressive agent against calcium-dependent NFAT activation that is also effective against asthmatic inflammation. However, the effects of FK506 on cysteine protease allergen-mediated airway inflammation remain unclear. In this study, we investigated the suppressive effects of FK506 on airway inflammation. FK506 had a partial inhibitory effect on ILC2-dependent eosinophil inflammation and a robust inhibitory effect on T cell-dependent eosinophil inflammation in a cysteine protease-induced mouse asthma model. The infiltration of T1/ST2<sup>+</sup> CD4 T cells in the lungs contributed to the persistence of eosinophil infiltration in the airway; FK506 completely inhibited the infiltration of T1/ST2<sup>+</sup> CD4 T cells. In the initial phase, FK506 treatment targeted lung ILC2 activation induced by leukotriene B<sub>4</sub> (LTB<sub>4</sub>)-mediated calcium signaling, but not IL-33 signaling. FK506 also inhibited the IL-13-dependent accumulation of T1/ST2<sup>+</sup> CD4 T cells in the lungs of the later responses. These results indicated that FK506 potently suppressed airway inflammation by targeting ILC2 activation and T1/ST2<sup>+</sup> CD4 T cell accumulation.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022","modification":"2024-11-12T01:59:17.843Z","creation":"2024-11-12T01:59:17.843Z"},"accession":"S-EPMC9683035","cross_references":{"pubmed":["36439133"],"doi":["10.3389/fimmu.2022.1014462"]}}