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Batf3-dependent type 1 dendritic cells drive the accumulation of lung resident memory CD4+ T cells

ABSTRACT: Tissue resident memory cells have recently emerged as a critically important cell type for both protective and pathogenic immune responses. In particular, these cells are required for allergen-induced airway hyperresponsiveness in animal models of allergic asthma. However, relatively little is known of the cellular and molecular mechanisms underlying the accumulation of these cells in the lung. Here, using gene targeted mice and MHC class II tetramers specific to clinically relevant house dust mite allergen, we show that allergen-specific resident memory CD4+ T cells are virtually absent in mice lacking Batf3, a transcription factor required for the development of type 1 lung dendritic cells. As a result, these animals display markedly reduced airway inflammation and very weak airway hyperresponsiveness in a house dust mite model of allergic asthma. Single cell RNA sequencing revealed that Batf3-deficient mice lack a subset of lung resident CD4+ T cells characterized by expression of the chemokine receptor-encoding gene, Cxcr6. Together, these data suggest that blocking the development or function of allergen-specific resident memory CD4+ T cells might be an effective approach to treat patients with allergic asthma.

ORGANISM(S): Mus musculus

PROVIDER: GSE277901 | GEO | 2025/07/09

REPOSITORIES: GEO

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Project description:Background: In asthma, airway epithelium remodeling can already be detected during childhood, and epithelial cells are more susceptible to virus and oxidative stress. Their exact role in natural history and severity of children allergic respiratory disease remains however surprisingly unexplored. Aim: To analyze dysfunctions of epithelium in dust mite allergic respiratory disease (rhinitis ¬± asthma) in children. Methods: Expression profilings of nasal epithelial cells collected by brushing were performed on Affymetrix Hugene 1.0 ST arrays. All allergic patients were sensitized to dust mite. 19 patients had an isolated allergic rhinitis (AR). 14 patients had AR associated with asthma. Patients were compared to 12 controls, their severity and control being assessed according to NAEPP and ARIA criteria. Infections by respiratory viruses were excluded by real-time PCR measurements. Results: 61 probes were able to distinguish allergic rhinitis children from healthy controls. A majority of these probes was under the control of Th2 cytokines, as evidenced by parallel experiments performed on primary cultures of nasal epithelial cells. In uncontrolled asthmatic patients, we observed not only an enhanced expression of these Th2-responsive transcripts, but also a down-regulation of interferon-responsive genes. Conclusion: Our study identifies a Th2 driven epithelial phenotype common to all dust mite allergic children. Besides, it suggests that epithelium is involved in the severity of the disease. Expression profiles observed in uncontrolled asthmatic patients suggest that severity of asthma is linked at the same time to atopy and to impaired viral response. Nasal epithelium gene expression profiling of dust mite allergic children with isolated rhinitis, rhinitis associated with asthma and controls. 38 samples classified in 4 categories : 14 isolated rhinitis (R), 6 rhinitis with uncontrolled asthma (UA), 7 rhinitis with controlled asthma (CA) and 11 healthy subjects (C )

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Batf3-dependent type 1 dendritic cells drive the accumulation of lung resident memory CD4+ T cells

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