Ulrich, Benjamin J.Kharwadkar, RakshinChu, MichellePajulas, AbigailMuralidharan, CharanyaKoh, ByungheeFu, YongyaoGao, HongyuHayes, Tristan A.Zhou, Hong-MingGoplen, Nick P.Nelson, Andrew S.Liu, YunlongLinnemann, Amelia K.Turner, Matthew J.Licona-Limón, PaulaFlavell, Richard A.Sun, JieKaplan, Mark H.2023-11-022023-11-022022Ulrich BJ, Kharwadkar R, Chu M, et al. Allergic airway recall responses require IL-9 from resident memory CD4+ T cells. Sci Immunol. 2022;7(69):eabg9296. doi:10.1126/sciimmunol.abg9296https://hdl.handle.net/1805/36898Asthma is a chronic inflammatory lung disease with intermittent flares predominately mediated through memory T cells. Yet, the identity of long-term memory cells that mediate allergic recall responses is not well defined. In this report, using a mouse model of chronic allergen exposure followed by an allergen-free rest period, we characterized a subpopulation of CD4+ T cells that secreted IL-9 as an obligate effector cytokine. IL-9-secreting cells had a resident memory T cell phenotype, and blocking IL-9 during a recall challenge or deleting IL-9 from T cells significantly diminished airway inflammation and airway hyperreactivity. T cells secreted IL-9 in an allergen recall-specific manner, and secretion was amplified by IL-33. Using scRNA-seq and scATAC-seq, we defined the cellular identity of a distinct population of T cells with a proallergic cytokine pattern. Thus, in a recall model of allergic airway inflammation, IL-9 secretion from a multicytokine-producing CD4+ T cell population was required for an allergen recall response.en-USPublisher PolicyAllergensAsthmaCytokinesHypersensitivityInflammationArticle