ArticleJCI insight2022
IRF4 expression by lung dendritic cells drives acute but not Trm cell-dependent memory Th2 responses.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Immunotherapy for asthma.Cellular & molecular immunology · 2025Review
- The immunology of asthma.Nature immunology · 2025Review
- Lung-resident memory CD4+ T cells are dependent on Batf3.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- IRF4-regulated transcriptional and functional heterogeneity of lung-resident CD11b+ cDC2 subsets during influenza virus infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- How type-2 dendritic cells induce Th2 differentiation: Instruction, repression, or fostering T cell-T cell communication?Allergy · 2025Review
- Overview of dendritic cells subsets and their involvement in immune-related pathological disease.BioImpacts : BI · 2025Review
- Emerging roles of MITF as a crucial regulator of immunity.Experimental & molecular medicine · 2024Review
- Catching Our Breath: Updates on the Role of Dendritic Cell Subsets in Asthma.Advanced biology · 2023Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Expression of the transcription factor interferon regulatory factor 4 (IRF4) is required for the development of lung conventional DCs type 2 (cDC2s) that elicit Th2 responses, yet how IRF4 functions in lung cDC2s throughout the acute and memory allergic response is not clear. Here, we used a mouse model that loses IRF4 expression after lung cDC2 development to demonstrate that mice with IRF4-deficient DCs display impaired memory responses to allergen. This defect in the memory response was a direct result of ineffective Th2 induction and impaired recruitment of activated effector T cells to the lung after sensitization. IRF4-deficient DCs demonstrated defects in their migration to the draining lymph node and in T cell priming. Finally, T cells primed by IRF4-competent DCs mediated potent memory responses independently of IRF4-expressing DCs, demonstrating that IRF4-expressing DCs are not necessary during the memory response. Thus, IRF4 controlled a program in mature DCs governing Th2 priming and effector responses, but IRF4-expressing DCs were dispensable during tissue-resident memory T cell-dependent memory responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.