ArticleThe British journal of dermatology2008
Transforming growth factor-beta/Smad3 signalling regulates inflammatory responses in a murine model of contact hypersensitivity.
Article in The British journal of dermatology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 40 citations in OpenAlex.
- Potential Supportive Effects of AP Collagen Peptides on Skin Hydration in a Mouse Model of Oxazolone-Induced Atopic Dermatitis.Journal of microbiology and biotechnology · 2026Article
- Impaired Molecular Mechanisms Contributing to Chronic Pain in Patients with Hidradenitis Suppurativa: Exploring Potential Biomarkers and Therapeutic Targets.International journal of molecular sciences · 2025Article
- Association of asthma genetic variants with asthma-associated traits reveals molecular pathways of eosinophilic asthma.Clinical and translational allergy · 2023Article
- Smad3 is essential for polarization of tumor-associated neutrophils in non-small cell lung carcinoma.Nature communications · 2023Article
- The Roles of Immunoregulatory Networks in Severe Drug Hypersensitivity.Frontiers in immunology · 2021Review
- M2-Type Macrophages Induce Tregs Generation by Activating the TGF-β/Smad Signalling Pathway to Promote Colorectal Cancer Development.OncoTargets and therapy · 2021Article
- CCL24 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021Article
- Shared genetic and experimental links between obesity-related traits and asthma subtypes in UK Biobank.The Journal of allergy and clinical immunology · 2020Article
- Serum interleukin-37 level and interleukin-37 gene polymorphism in patients with Behçet disease.Clinical rheumatology · 2019Article
- Assessment of tumor growth factor-β1 neutralizing antibody in the treatment of allergic rhinitis and asthma.Experimental and therapeutic medicine · 2018Article
- Epigenome-wide analysis links SMAD3 methylation at birth to asthma in children of asthmatic mothers.The Journal of allergy and clinical immunology · 2017Article
- Article
- Association of the Smad3 and NFATc2 gene polymorphisms and their serum levels with susceptibility to rheumatoid arthritis in Polish cohorts.Clinical and experimental immunology · 2015Article
- Decorin potentiates interferon-γ activity in a model of allergic inflammation.The Journal of biological chemistry · 2013Article
- Role of Th17 cells in skin inflammation of allergic contact dermatitis.Clinical & developmental immunology · 2013Review
- Histopathological features and expression profiles of cytokines, chemokines and SOCS family proteins in trehalose 6,6'-dimycolate-induced granulomatous lesions.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2011Article
- Loss of expression of TGF-βs and their receptors in chronic skin lesions induced by sulfur mustard as compared with chronic contact dermatitis patients.BMC dermatology · 2011Article
- Role of SMAD and non-SMAD signals in the development of Th17 and regulatory T cells.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTransforming growth factor (TGF)-beta is an important modulator of immune functions and cellular responses, such as differentiation, proliferation, migration and apoptosis. The Smad proteins, which are intracellular TGF-beta signal transducers, mediate most actions of TGF-beta.
objectivesThis study examines the role of Smad3 in a murine model of contact hypersensitivity (CHS).
methodsThe CHS response to oxazolone was studied in Smad3-deficient mice. The ear swelling response was measured and skin biopsies from oxazolone-sensitized skin areas were obtained for RNA isolation, immunohistochemical analyses and histology. Ear draining lymph nodes were collected for RNA isolation and proliferation tests. Quantitative real-time polymerase chain reaction was used to quantify mRNA expression of cytokines, chemokines and transcription factors. Results The expression of proinflammatory [interleukin (IL)-1beta, tumour necrosis factor-alpha, IL-6], Th2 (IL-4) and Th17 type cytokines (IL-17), as well as regulatory components (TGF-beta, Foxp3) increased significantly at the mRNA level in the skin of oxazolone-treated Smad3-/- mice when compared with wild-type controls. The expression of the Th1 type cytokine IFN-gamma and the chemokines CXCL9 and CXCL10 was, however, unaffected by the lack of Smad3. The number of neutrophils and expression of the chemokines CCL3 and CXCL5, which are both involved in neutrophil recruitment, were increased in mice lacking Smad3. Also Th2 type chemokines CCL24, CCL3 and CXCL5 were increased in the skin of Smad3-/- mice compared with wild-type mice. In the lymph nodes, mRNA of IL-1beta and IL-17, but not IL-4, TGF-beta or Foxp3, was increased in Smad3-/- mice during the CHS response.
conclusionsThe lack of intact TGF-beta signalling via Smad3 results in an increased proinflammatory, Th2 and Th17 type response in the skin, as well as increased expression of regulatory elements such as TGF-beta and Foxp3. Understanding the role of Smad3 in the CHS response may offer treatment and prevention strategies in this often disabling disease.
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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.