ReviewFrontiers in immunology2019
Type1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis.
Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 87 citations in OpenAlex.
- Dental pulp stem cell-derived exosomes attenuate psoriatic inflammation by restoring epithelial redox homeostasis via a miR-1246/miR-17-3p-GPX2-NF-κB axis.Stem cell research & therapy · 2026Article
- Inflammatory burden and cardiovascular risk stratification across psoriasis severity stages.Journal of medicine and life · 2026Article
- Type I interferon signaling defines a novel disease signature in xeroderma pigmentosum C human keratinocytes.Scientific reports · 2026Article
- Linear psoriasis and Koebner phenomenon: A review.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2026Review
- Type I interferon in psoriasis: mechanisms and clinical implications.Frontiers in immunology · 2026Review
- RadiotherapyTranslational lung cancer research · 2025Article
- Interferons in Autoimmunity: From Loss of Tolerance to Chronic Inflammation.Biomedicines · 2025Review
- Transcriptomic Differences Between Immortalized Oral and Skin Keratinocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The CARD14Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Exploring precision treatments in immune-mediated inflammatory diseases: Harnessing the infinite potential of nucleic acid delivery.Exploration (Beijing, China) · 2025Review
- Paucity of viral infection symptoms in patients with immune-mediated inflammatory diseases.BMJ open · 2025Article
- Bilayered skin equivalent mimicking psoriasis as predictive tool for preclinical treatment studies.Communications biology · 2024Article
- The Role of Vitamin D3 Deficiency and Colonization of the Oral Mucosa byJournal of clinical medicine · 2024Review
- Article
- Triggers for the onset and recurrence of psoriasis: a review and update.Cell communication and signaling : CCS · 2024Review
- Adalimumab induced psoriasis in Crohn's disease and treatment with ustekinumab: case report and special histopathological findings.Frontiers in medicine · 2024Article
- Can Biologic Agents Improve Treatment Success in Obese Patients With Psoriasis Vulgaris: A Retrospective Review of 320 Patients With Psoriasis Vulgaris.Dermatology practical & conceptual · 2024Article
- Signaling pathways and targeted therapies for psoriasis.Signal transduction and targeted therapy · 2023Review
- Inflammation and Psoriasis: A Comprehensive Review.International journal of molecular sciences · 2023Review
- The Crucial Roles and Research Advances of cGAS-STING Pathway in Cutaneous Disorders.Inflammation · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 2 countries.
Funding
Abstract
Psoriasis is a chronic autoimmune skin disease that can often be triggered upon skin injury, known as Koebner phenomenon. Type 1 interferons (IFNα and IFNβ), key cytokines that activate autoimmunity during viral infection, have been suggested to play an indispensable role in initiating psoriasis during skin injury. Type 1 IFN-inducible gene signature has been identified as one of the major upregulated gene signatures in psoriatic skin. Type 1 IFNs treatments often directly induce or exacerbate psoriasis, whereas blocking type 1 IFNs signaling pathway in animal models effectively inhibits the development of T cell-mediated skin inflammation and psoriasis-like inflammatory diseases. Epidermal keratinocytes (KCs) occupy the outermost position in the skin and are the first responder to skin injury. Skin injury rapidly induces IFNβ from KCs and IFNα from dermal plasmacytoid dendritic cells (pDCs) through distinct mechanisms. Host antimicrobial peptide LL37 potentiates double-stranded RNA (dsRNA) immune pathways in keratinocytes and single-stranded RNA or DNA pathways in pDCs, leading to production of distinct type 1 IFN genes. IFNβ from KC promotes dendritic cell maturation and the subsequent T cell proliferation, contributing to autoimmune activation during skin injury and psoriasis pathogenesis. Accumulating evidences have indicated an important role of this dsRNA immune pathway in psoriasis pathogenesis. Together, this review describes how skin injury induces type 1 IFNs from skin cells and how this may initiate autoimmune cascades that trigger psoriasis. Targeting keratinocytes or type 1 IFNs in combination with T cell therapy may result in more sustainable effect to treat auto-inflammatory skin diseases such as psoriasis.
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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.