ArticleThe Journal of investigative dermatology2009
Inflammatory skin disease in K5.hTGF-beta1 transgenic mice is not dependent on the IL-23/Th17 inflammatory pathway.
Article in The Journal of investigative dermatology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 35 citations in OpenAlex.
- Modulation of the KEAP1-NRF2 pathway by Erianin: A novel approach to reduce psoriasiform inflammation and inflammatory signaling.Open life sciences · 2025Article
- The mode of action of IL-23 in experimental inflammatory arthritic pain and disease.Arthritis research & therapy · 2024Article
- Transforming growth factor β--at the centre of systemic sclerosis.Nature reviews. Rheumatology · 2014Review
- Accumulation of FLT3(+) CD11c (+) dendritic cells in psoriatic lesions and the anti-psoriatic effect of a selective FLT3 inhibitor.Immunologic research · 2014Article
- Functional conservation of Gsdma cluster genes specifically duplicated in the mouse genome.G3 (Bethesda, Md.) · 2013Article
- TGFβ1 overexpression by keratinocytes alters skin dendritic cell homeostasis and enhances contact hypersensitivity.The Journal of investigative dermatology · 2013Article
- The pro-inflammatory role of TGFβ1: a paradox?International journal of biological sciences · 2012Review
- The Role of TGFβ Signaling in Squamous Cell Cancer: Lessons from Mouse Models.Journal of skin cancer · 2012Article
- Platelet-activating factor blockade inhibits the T-helper type 17 cell pathway and suppresses psoriasis-like skin disease in K5.hTGF-β1 transgenic mice.The American journal of pathology · 2011Article
- Article
- The potential role of Th17 lymphocytes in patients with psoriasis.Anais brasileiros de dermatologiaArticle
- Plasma Levels of Interleukin-17, Interleukin-23, and Transforming Growth Factor-β in Sudanese Patients with Vitiligo: A Case-Control Study.Indian journal of dermatologyArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
In the presence of IL-6, transforming growth factor (TGF)-beta1 induces differentiation of T helper (Th) 17 cells in mice. Interleukin (IL)-23, a heterodimeric cytokine composed of IL-23p19 and IL-12/23p40 subunits, stimulates the growth and expansion of Th17 cells, and has been implicated in psoriasis pathogenesis. To study the associations between TGF-beta1, the IL-23/Th17 inflammatory pathway, and psoriasis, we investigated inflammatory skin disease in transgenic mice that constitutively overexpress human TGF-beta1 in basal keratinocytes (K5.hTGF-beta1 transgenic mice); these mice had previously been reported as having a psoriasis-like disease. K5.hTGF-beta1 transgenic mice had high levels of TGF-beta1 mRNA and protein in both skin and serum. Levels of cytokines involved in IL-23/Th17-mediated inflammation were not elevated in lesional skin compared with those in non-lesional and wild-type skin. It is noteworthy that IL-4 and IgE were markedly elevated in inflamed skin and serum, respectively, of transgenic mice. Monoclonal antibodies (mAbs) specifically directed against IL-23p19 or IL-12/23p40 had no clinical effect on established inflammatory skin disease in K5.hTGF-beta1 transgenic mice, whereas the same mAbs were able to block the development of murine experimental autoimmune encephalomyelitis, an IL-23/Th17-mediated disease. In summary, the IL-23/Th17 inflammatory pathway is not responsible for the maintenance of inflammatory skin disease in K5.hTGF-beta1 transgenic mice.
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