ArticleMolecular medicine reports2016
Influence of different types of contact hypersensitivity on imiquimod-induced psoriasis-like inflammation in mice.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Dermal adipogenesis protects against neutrophilic skin inflammation during psoriasis pathogenesis.Cellular & molecular immunology · 2025Article
- Evaluation of Clobetasol and Tacrolimus Treatments in an Imiquimod-Induced Psoriasis Rat Model.International journal of molecular sciences · 2024Article
- Inflammatory Cues Direct Skin-Resident Type 1 Innate Lymphoid Cells to Adopt a Psoriasis-Promoting Identity.JID innovations : skin science from molecules to population health · 2023Article
- Inhibition of DYRK1B suppresses inflammation in allergic contact dermatitis model and Th1/Th17 immune response.Scientific reports · 2023Article
- ProbioticFrontiers in microbiology · 2018Article
- Overexpression and potential roles of NRIP1 in psoriasis.Oncotarget · 2016Article
- Evaluation of the profile of inflammatory cytokines, through immunohistochemistry, in the skin of patients with allergic contact dermatitis to nickel in the acute and chronic phases.Anais brasileiros de dermatologiaObservational
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is currently believed that psoriasis and allergic contact dermatitis (ACD) are different diseases; however, they share clinical similarities. The involvement of T helper 17 (Th17) cells in these disorders provides a novel opportunity to investigate the relationship between them. The present study aimed to determine whether the same or overlapping inflammatory pathways are involved in the two diseases, and the influence of different types of ACD on psoriasis. Compound mouse models of Th1 or Th2‑type contact hypersensitivity (CHS) combined with imiquimod (IMQ)‑induced psoriasis‑like inflammation were established, in order to mimic the characteristics of ACD and psoriasis. Histopathology, immunohistochemistry and cytokine detection in blood serum and tissues were used to compare the differences between the mice treated with IMQ alone or IMQ combined with Th1 and Th2‑type CHS. As compared with the IMQ‑treated mice or IMQ-treated Th1‑type CHS mice, the mice with Th2‑type CHS treated with IMQ exhibited more serious psoriasis‑like inflammation with increased epidermal thickness and infiltrating cells in the derma. High mRNA expression levels of interleukin (IL)‑17, IL‑22, IL‑23, TNF‑α and RORγt were detected in back skin lesions. Additionally, high levels of IL‑17 and IL‑22 in blood serum were detected in IMQ‑treated mice combined with Th2‑type CHS. The mice treated with IMQ alone, and IMQ treatment combined with Th1‑type CHS had a comparable psoriasis‑like inflammatory response in the back skin. In conclusion, these data demonstrate that Th2‑type CHS exacerbated the IMQ‑treated psoriatic inflammation of mice via the IL‑23/IL‑17 axis. Th17 cells and associated pathways may link ACD and psoriasis. Therefore, patients with psoriasis should avoid contact with specific sensitizers, such as fragrance and rubber products, which may induce Th2 polarization.
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