ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
STAT6 regulates natural helper cell proliferation during lung inflammation initiated by Alternaria.
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
107 citing papers in PubMed, 157 citations in OpenAlex.
- Article
- Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026Review
- Acute stress alleviates type 2 lung inflammation by restricting ILC2s through corticosterone-glucocorticoid receptor signaling.Cellular & molecular immunology · 2026Article
- STAT4 drives optimal expansion and transcriptional repression of type I interferon pathway in inflammatory ILC2.Cellular and molecular life sciences : CMLS · 2026Article
- STAT6-IP-dependent inhibition of type 2 innate and Th2 adaptive immunity in the murine lung.ImmunoHorizons · 2026Article
- CBX7 functions as a methylation-dependent inducer of gene transcription and regulator of cytosolic signaling in lymphoid cells.Science advances · 2026Article
- Innate airway immune response to fungal allergens.Frontiers in immunology · 2026Review
- Chronic Inflammation in Asthma: Looking Beyond the Th2 Cell.Immunological reviews · 2025Review
- E3 ligase RNF128 restricts A. alternata-induced ILC2 activation and type 2 immune response in the murine lung.Scientific reports · 2025Article
- Comprehensive sequencing of the lung neuroimmune landscape in response to asthmatic induction.Frontiers in immunology · 2025Article
- PIP-seq identifies novel heterogeneous lung innate lymphocyte population activation after combustion product exposure.Scientific reports · 2024Article
- Type 2 Innate Lymphoid Cells and Skin Fibrosis in a Murine Model of Atopic Dermatitis-Like Skin Inflammation.Journal of Korean medical science · 2024Article
- Administration of a bacterial lysate to the airway compartment is sufficient to inhibit allergen-induced lung eosinophilia in germ-free mice.Journal of leukocyte biology · 2024Article
- TL1A is an epithelial alarmin that cooperates with IL-33 for initiation of allergic airway inflammation.The Journal of experimental medicine · 2024Article
- Cholinergic sensing of allergen exposure by airway epithelium promotes type 2 immunity in the lungs.The Journal of allergy and clinical immunology · 2024Article
- A nasal cell atlas reveals heterogeneity of tuft cells and their role in directing olfactory stem cell proliferation.Science immunology · 2024Article
- Article
- JAK3 inhibitor suppresses multipotent ILC2s and attenuates steroid-resistant asthma.Science advances · 2023Article
- ATP functions as a primary alarmin in allergen-induced type 2 immunity.American journal of physiology. Cell physiology · 2023Review
- Solar ultraviolet B radiation promotes α-MSH secretion to attenuate the function of ILC2s via the pituitary-lung axis.Nature communications · 2023Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Asthma exacerbations can be caused by a number of factors, including the fungal allergen Alternaria, which is specifically associated with severe and near-fatal attacks. The mechanisms that trigger lung responses are unclear and might vary between allergens. A comparison between Alternaria, Aspergillus, Candida, and house dust mite, all allergens in humans, showed that only Alternaria promoted immediate innate airway eosinophilia within 12 h of inhalation in nonsensitized mice. Alternaria, but not the other allergens, induced a rapid increase in airway levels of IL-33, accompanied by IL-33 receptor (IL-33R)-positive natural helper cell (NHC) production of IL-5 and IL-13. NHCs in the lung and bone marrow constitutively expressed transcription factors [GATA-3 and E26 transformation-specific sequence-1 (ETS-1)] that could allow for rapid induction of T helper type 2 (Th2) cytokines. Lung NHC numbers and proliferation (%Ki-67), but not IL-5 or GATA-3 expression, were significantly reduced in STAT6-deficient mice 3 days after one challenge with Alternaria. Alternaria induced NHC expression of the EGF receptor ligand amphiregulin (partially dependent on STAT6), as well as EGF receptor signaling in the airway epithelium. Finally, human peripheral blood NHCs (CRTH2(+)CD127(+) lineage-negative lymphocytes) from allergic individuals highly expressed GATA-3 and ETS-1, similar to lung NHCs in mice. In summary, Alternaria-induced lung NHC proliferation and expression of amphiregulin are regulated by STAT6. In addition, NHCs in mouse and humans are primed to express Th2 cytokines through constitutive expression of GATA-3 and ETS-1. Thus several transcription factor pathways (STAT6, GATA-3, and ETS-1) may contribute to NHC proliferation and Th2-type responses in Alternaria-induced asthma.
Indexed as
Identifiers
What OpenQuestion holds
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.