ArticleJournal of immunology (Baltimore, Md. : 1950)2025
Lung-resident memory CD4+ T cells are dependent on Batf3.
Article in Journal of immunology (Baltimore, Md. : 1950), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- SC-framework: A robust and FAIR semi-interactive environment for single-cell resolution datasets.iScience · 2026Article
- Neutrophil Antigen Presentation Reprograms the Tumor Microenvironment and Elicits Durable and Broad Antitumor Immunity.Cancer research communications · 2026Article
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Authors and funding
7 authors.
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Abstract
Tissue-resident memory cells contribute to allergen-induced inflammation and airway hyperresponsiveness, but relatively little is known of the cellular and molecular mechanisms underlying the accumulation of these cells in the lung. Here, we show that allergen-specific CD4+ resident memory T cells are virtually absent in lungs of mice lacking Batf3, a transcription factor required for the development of type 1 lung dendritic cells (cDC1). These animals become sensitized to inhaled allergens and display normal responses in a short-term house dust mite-dependent model of asthma. However, they have strongly reduced airway inflammation and weak airway hyperresponsiveness in a similar, but long-term model of 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 show that Batf3 promotes the development of CD4+ resident memory T cells and thus allergic responses to inhaled allergens.
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