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TSLP and IL-33 reciprocally promote each other's lung protein expression and ILC2 receptor expression to enhance innate type-2 airway inflammation

dc.contributor.authorToki, Shinji
dc.contributor.authorGoleniewska, Kasia
dc.contributor.authorZhang, Jian
dc.contributor.authorZhou, Weisong
dc.contributor.authorNewcomb, Dawn C.
dc.contributor.authorZhou, Baohua
dc.contributor.authorKita, Hirohito
dc.contributor.authorBoyd, Kelli L.
dc.contributor.authorPeebles, Ray S., Jr.
dc.date.accessioned2020-10-22T19:30:02Z
dc.date.available2020-10-22T19:30:02Z
dc.date.issued2020-02
dc.identifier.citationToki, S., Goleniewska, K., Zhang, J., Zhou, W., Newcomb, D. C., Zhou, B., Kita, H., Boyd, K. L., & Peebles, R. S., Jr (2020). TSLP and IL-33 reciprocally promote each other's lung protein expression and ILC2 receptor expression to enhance innate type-2 airway inflammation. Allergy, 75(7), 1606–1617. https://doi.org/10.1111/all.14196en_US
dc.identifier.issn0105-4538
dc.identifier.urihttp://hdl.handle.net/1803/16247
dc.description.abstractBackground The epithelial cell-derived danger signal mediators thymic stromal lymphopoietin (TSLP) and IL-33 are consistently associated with adaptive Th2 immune responses in asthma. In addition, TSLP and IL-33 synergistically promoted group 2 innate lymphoid cell (ILC2) activation to induce innate allergic inflammation. However, the mechanism of this synergistic ILC2 activation is unknown. Methods BALB/c WT and TSLP receptor-deficient (TSLPR-/-) mice were challenged intranasally with Alternaria extract (Alt-Ext) or PBS for 4 consecutive days to evaluate innate airway allergic inflammation. WT mice pre-administered with rTSLP or vehicle, TSLPR-/- mice, and IL-33 receptor-deficient (ST2(-/-)) mice were challenged intranasally with Alt-Ext or vehicle once or twice to evaluate IL-33 release and TSLP expression in the lung. TSLPR and ST2 expression on lung ILC2 were measured by flow cytometry after treatment of rTSLP, rIL-33, rTSLP + rIL-33, or vehicle. Results Thymic stromal lymphopoietin receptor deficient mice had significantly decreased the number of lung ILC2 expressing IL-5 and IL-13 following Alt-Ext-challenge compared to WT mice. Further, eosinophilia, protein level of lung IL-4, IL-5, and IL-13, and airway mucus score were also significantly decreased in TSLPR-/- mice compared to WT mice. Endogenous and exogenous TSLP increased Alt-Ext-induced IL-33 release into BALF, and ST2 deficiency decreased Alt-Ext-induced TSLP expression in the lung. Further, rTSLP and rIL-33 treatment reciprocally increased each other's receptor expression on lung ILC2 in vivo and in vitro. Conclusion Thymic stromal lymphopoietin and IL-33 signaling reciprocally enhanced each other's protein release and expression in the lung following Alt-Ext-challenge and each other's receptor expression on lung ILC2 to enhance ILC2 activation.en_US
dc.description.sponsorshipNIH, Grant/Award Number: R01AI111820, R01AI124456, R01AI145265, R21AI145397 and U19AI095227; U.S. Department of Veterans Affairs, Grant/Award Number: I01BX004299en_US
dc.language.isoen_USen_US
dc.publisherAllergyen_US
dc.rightsCopyright © 2020 The Authors. Allergy published by John Wiley & Sons Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
dc.source.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7354889/
dc.subjectGroup 2 innate lymphoid cells (ILC2en_US
dc.subjectGroup 2 innate lymphoid cells (ILC2)en_US
dc.subjectIL-33en_US
dc.subjectTSLPen_US
dc.titleTSLP and IL-33 reciprocally promote each other's lung protein expression and ILC2 receptor expression to enhance innate type-2 airway inflammationen_US
dc.typeArticleen_US
dc.identifier.doi10.1111/all.14196


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