ArticleMucosal immunology2023
Unfolded protein response factor ATF6 augments T helper cell responses and promotes mixed granulocytic airway inflammation.
Article in Mucosal immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 15 citations in OpenAlex.
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- Human LY9 governs CD4Science immunology · 2025Article
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- Unfolded protein responses: Dynamic machinery in wound healing.Pharmacology & therapeutics · 2025Review
- T cell heterogeneity in asthma pathogenesis: from immunological mechanisms to biological targeted therapies.Frontiers in immunology · 2025Review
- Corticosterone effects induced by stress and immunity and inflammation: mechanisms of communication.Frontiers in endocrinology · 2025Review
- Elevated SerpinB2 regulates MUC5AC expression via STAT6 signaling in nasal epithelial cells in allergic rhinitis.Frontiers in immunology · 2025Article
- Unconventional Activation of IRE1 Enhances Th17 Responses and Promotes Airway Neutrophilia.American journal of respiratory cell and molecular biology · 2024Article
- Unfolding the Role of Th17 Cells in Neutrophilic Lung Inflammation.American journal of respiratory cell and molecular biology · 2024Article
- RNA sequencing reveals dynamic expression of genes related to innate immune responses in canine small intestinal epithelial cells induced byFrontiers in veterinary science · 2024Article
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
The unfolded protein response (UPR) is associated with the risk of asthma, including treatment-refractory severe asthma. Recent studies demonstrated a pathogenic role of activating transcription factor 6a (ATF6a or ATF6), an essential UPR sensor, in airway structural cells. However, its role in T helper (TH) cells has not been well examined. In this study, we found that ATF6 was selectively induced by signal transducer and activator of transcription6 (STAT6) and STAT3 in TH2 and TH17 cells, respectively. ATF6 upregulated UPR genes and promoted the differentiation and cytokine secretion of TH2 and TH17 cells. T cell-specific Atf6-deficiency impaired TH2 and TH17 responses in vitro and in vivo and attenuated mixed granulocytic experimental asthma. ATF6 inhibitor Ceapin A7 suppressed the expression of ATF6 downstream genes and TH cell cytokines by both murine and human memory clusters of differentiation 4 (CD4)
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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.