ArticleInternational journal of molecular sciences2019
Human IL-23R Cytokine-Binding Homology Region-Fc Fusion Protein Ameliorates Psoriasis via the Decrease of Systemic Th17 and ILC3 Cell Responses.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- ILC3s as central regulators of mucosal homeostasis and disease pathogenesis (Review).International journal of molecular medicine · 2026Review
- Macrophage INSIG1 deficiency drives psoriasiform dermatitis via the SREBP2-STAT1 axis.Nature communications · 2026Article
- Understanding Type 3 Innate Lymphoid Cells and Crosstalk with the Microbiota: A Skin Connection.International journal of molecular sciences · 2024Review
- Comparative studies on mannan and imiquimod induced experimental plaque psoriasis inflammation in inbred mice.Clinical and experimental immunology · 2023Article
- ILC3: a case of conflicted identity.Frontiers in immunology · 2023Review
- The regulatory mechanism and potential application of IL-23 in autoimmune diseases.Frontiers in pharmacology · 2022Review
- Interleukin 23 and autoimmune diseases: current and possible future therapies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Interleukin (IL)-23 is considered an effective therapeutic target for the treatment of psoriasis because of the crucial role of the IL-23/IL-17 axis in the pathogenesis of psoriasis, and it has recently been reported to be involved in ILC3 cell differentiation. In this study, we report that eukaryotically expressed rhIL23R-CHR/Fc, as an endogenous extracellular receptor analogue, could be a natural antagonist in an imiquimod (IMQ)-induced psoriasis-like mouse model, including the antagonizing effect of suppressed inflammation in the skin lesion, decreased production of pro-inflammatory cells, and reduced the expression of pro-inflammatory factors. The rhIL23R-CHR/Fc fusion protein inhibits both innate immune and adaptive immune-mediated inflammatory responses. These findings shed light on rhIL23R-CHR/Fc as a promising candidate therapy for the treatment of psoriasis.
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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.