IL-9 and Blimp-1 protects the transcriptional identity of group 2 innate lymphocytes in allergic asthma
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Updated: May 9, 2025

Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
Published on: May 10, 2022
Yibo Zheng1,2, Jinyi Zhang1,2, Aaron Yang1,3
1Center for Systems Immunology, Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Abstract:
Allergic asthma is driven by type 2 immune cells including type 2 innate lymphoid cells (ILC2s). ILC2s respond to the tissue alarmins IL-33 and IL-25, however these signals do not uniquely promote type 2 inflammation, and the factors that maintain ILC2s ability to produce type 2 cytokines are not known. Here, we show that allergen-driven tissue alarmins IL-33 and IL-25 rapidly induce IL-9, which directly upregulates the transcriptional repressor Blimp-1 through an autocrine/paracrine mechanism. Blimp-1 promotes type 2 responses by directly repressing type 1 inflammation including the cytokines IFNγ and TNF. Deletion of Blimp-1 in ILC2s increases type 1 cytokines and concomitantly reduces type 2 cytokines, ameliorating mucus production and airway inflammation in response to allergens. Thus, Blimp-1 maintains the type 2 transcriptional identity of ILC2s in response to inflammation, driving type 2 immunity and allergic asthma.
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