Allergic airway recall responses require IL-9 from resident memory CD4+ T cells

Benjamin J. Ulrich, Rakshin Kharwadkar, Michelle Chu, Abigail Pajulas, Charanya Muralidharan, Byunghee Koh, Yongyao Fu, Hongyu Gao, Tristan A. Hayes, Hong Ming Zhou, Nick P. Goplen, Andrew S. Nelson, Yunlong Liu, Amelia K. Linnemann, Matthew J. Turner, Paula Licona-Limón, Richard A. Flavell, Jie Sun, Mark H. Kaplan

Research output: Contribution to journalArticlepeer-review


Asthma 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.

Original languageEnglish (US)
Article numbereabg9296
JournalScience Immunology
Issue number69
StatePublished - Mar 2022

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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