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Therefore, we hypothesized that signaling through the endogenous GLP\u20101R and the GIPR individually decreases allergic airway inflammation and that the combination of GLP\u20101R and GIPR signaling together additively inhibits allergen\u2010induced lung and airway inflammation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>WT (C57BL\/6J), GLP\u20101R knockout (KO), GIPR KO, and GLP\u20101R\/GIPR double KO (DKO) mice were challenged intranasally with <jats:italic>Alternaria alternata<\/jats:italic> extract (Alt\u2010Ext) or vehicle to evaluate the impact of signaling through these receptors on the innate allergen\u2010induced inflammatory response that is primarily driven by group 2 innate lymphoid cells (ILC2).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Alt\u2010Ext\u2010induced IL\u201033 release in the bronchoalveolar lavage fluid (BALF) was not different between the mouse strains, but thymic stromal lymphopoietin (TSLP) was significantly increased in GLP\u20101R\/GIPR DKO mice challenged with Alt\u2010Ext compared to the other strains. Furthermore, Alt\u2010Ext\u2010induced protein expression of IL\u20105, IL\u201013, CCL11, and CCL24 in the lung homogenates, the number of eosinophils, lymphocytes, and neutrophils in the BALF, and the number of lung GATA3+ ILC2 were significantly increased in GLP\u20101R\/GIPR DKO mice compared to the other 3 strains. Furthermore, ICAM\u20101 expression on lung epithelial cells was increased in GLP\u20101R\/GIPR DKO mice challenged with Alt\u2010Ext compared to the other 3 strains.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Deficiency of both GLP\u20101R and GIPR signaling together increased TSLP release, ILC2 activation, and early type 2 innate immune responses to aeroallergen exposure. Combined GLP\u20101R and GIPR signaling should be explored for the treatment of asthma.<\/jats:p><\/jats:sec>","DOI":"10.1111\/all.16402","type":"journal-article","created":{"date-parts":[[2024,11,19]],"date-time":"2024-11-19T11:03:00Z","timestamp":1732014180000},"page":"3373-3384","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Endogenous Glucagon\u2010Like Peptide\u20101 Receptor and Glucose\u2010Dependent Insulinotropic Polypeptide Receptor Signaling Inhibits Aeroallergen\u2010Induced Innate Airway Inflammation"],"prefix":"10.1111","volume":"79","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4379-9118","authenticated-orcid":false,"given":"Shinji","family":"Toki","sequence":"first","affiliation":[{"name":"Division of Allergy, Pulmonary, and Critical Care Medicine Vanderbilt University School of Medicine  Nashville Tennessee 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