ArticleJournal of immunology (Baltimore, Md. : 1950)2011
STAT6 expression in multiple cell types mediates the cooperative development of allergic airway disease.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Regulation of eosinophil recruitment and heterogeneity during allergic airway inflammation.Frontiers in allergy · 2025Review
- Plexin B1 controls Treg numbers, limits allergic airway inflammation, and regulates mucins.Frontiers in immunology · 2023Article
- STAT6-Dependent Exacerbation of House Dust Mite-Induced Allergic Airway Disease in Mice by Multi-Walled Carbon Nanotubes.NanoImpact · 2021Article
- Semaphorin3E/plexinD1 Axis in Asthma: What We Know So Far!Advances in experimental medicine and biology · 2021Article
- IL-27 signaling deficiency develops Th17-enhanced Th2-dominant inflammation in murine allergic conjunctivitis model.Allergy · 2019Article
- The Expression Levels of IL-4/IL-13/STAT6 Signaling Pathway Genes and SOCS3 Could Help to Differentiate the Histopathological Subtypes of Non-Small Cell Lung Carcinoma.Molecular diagnosis & therapy · 2018Article
- IL-4 and IL-13 Receptor Signaling From 4PS to Insulin Receptor Substrate 2: There and Back Again, a Historical View.Frontiers in immunology · 2018Review
- Molecular Mechanisms of Airway Hyperresponsiveness in a Murine Model of Steroid-Resistant Airway Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Cutting edge: STAT6 signaling in eosinophils is necessary for development of allergic airway inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Regulatory tone and mucosal immunity in asthma.International immunopharmacology · 2014Review
- TSLP induces mast cell development and aggravates allergic reactions through the activation of MDM2 and STAT6.The Journal of investigative dermatology · 2014Article
- Neuroimmune semaphorin 4D is necessary for optimal lung allergic inflammation.Molecular immunology · 2013Article
- Neuroimmune semaphorin 4A as a drug and drug target for asthma.International immunopharmacology · 2013Article
- STAT6 and lung inflammation.JAK-STAT · 2013Review
- STAT6 controls the number of regulatory T cells in vivo, thereby regulating allergic lung inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Therapeutic modulators of STAT signalling for human diseases.Nature reviews. Drug discovery · 2013Review
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- Neuroimmune semaphorin 4A downregulates the severity of allergic response.Mucosal immunology · 2012Article
- Adoptive transfer of IL-4Rα+ macrophages is sufficient to enhance eosinophilic inflammation in a mouse model of allergic lung inflammation.BMC immunology · 2012Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Th2 cells induce asthma through the secretion of cytokines. Two such cytokines, IL-4 and IL-13, are critical mediators of many features of this disease. They both share a common receptor subunit, IL-4Rα, and signal through the STAT6 pathway. STAT6(-/-) mice have impaired Th2 differentiation and reduced airway response to allergen. Transferred Th2 cells were not able to elicit eosinophilia in response to OVA in STAT6(-/-) mice. To clarify the role of STAT6 in allergic airway inflammation, we generated mouse bone marrow (BM) chimeras. We observed little to no eosinophilia in OVA-treated STAT6(-/-) mice even when STAT6(+/+) BM or Th2 cells were provided. However, when Th2 cells were transferred to STAT6×Rag2(-/-) mice, we observed an eosinophilic response to OVA. Nevertheless, the expression of STAT6 on either BM-derived cells or lung resident cells enhanced the severity of OVA-induced eosinophilia. Moreover, when both the BM donor and recipient lacked lymphocytes, transferred Th2 cells were sufficient to induce the level of eosinophilia comparable with that of wild-type (WT) mice. The expression of STAT6 in BM-derived cells was more critical for the enhanced eosinophilic response. Furthermore, we found a significantly higher number of CD4(+)CD25(+)Foxp3(+) T cells (regulatory T cells [Tregs]) in PBS- and OVA-treated STAT6(-/-) mouse lungs compared with that in WT animals suggesting that STAT6 limits both naturally occurring and Ag-induced Tregs. Tregs obtained from either WT or STAT6(-/-) mice were equally efficient in suppressing CD4(+) T cell proliferation in vitro. Taken together, our studies demonstrate multiple STAT6-dependent and -independent features of allergic inflammation, which may impact treatments targeting STAT6.
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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.