ArticleNature immunology2022
IL-17D-induced inhibition of DDX5 expression in keratinocytes amplifies IL-36R-mediated skin inflammation.
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Article in Nature immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 45 papers.
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45citing papers in PubMed
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Who cites it
45 citing papers in PubMed.
- Atezolizumab plus bevacizumab in patients with unresectable or metastatic mucosal melanoma: 3-year survival update and multi-omics analysis.Clinical and translational medicine · 2025Trial
- DDX5 (p68) and UbE2T as emerging superior cancer therapeutic targets: dual molecular glue target degradation by FL118 for conquering difficult-to-treat cancers.Journal of experimental & clinical cancer research : CR · 2026Review
- Targeting microglial C1q alleviates blood-brain barrier disruption in the thalamus after cortical infarction.Journal of neuroinflammation · 2026Article
- Aged skin exacerbates experimental osteoarthritis via enhanced IL-36R signaling.Nature communications · 2026Article
- N4BP1 acts as a potent negative regulator of IL-17 signaling by blocking the translation of Act1 mRNA.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- IL-27 signaling mediates skin inflammation in experimental psoriasis and atopic dermatitis.Cell & bioscience · 2026Article
- STAT3 ablation in keratinocytes ameliorates allergic contact dermatitis in DNCB-induced mice model.Iranian journal of basic medical sciences · 2026Article
- Unveiling Interleukin-40: A Novel Regulator of Macrophage and B Cell Function in Allergic Asthma.International journal of biological sciences · 2026Article
- Inhibition of DDX5-Mediated G-Quadruplex Unwinding in the β-Catenin 5'-UTR by Magnesium Isoglycyrrhizinate Alleviates Chemotherapy-Induced Intestinal Injury.Research (Washington, D.C.) · 2026Article
- Amelioration of psoriasis-like skin lesions by human amniotic mesenchymal stem cells: insights from multiomics profiling in mice.Frontiers in immunology · 2026Article
- Yin-Hua Li-Shi Formula Exerts Anti-Atopic Dermatitis Effects Through Luteolin Targeting AKT/MAPK-IL-6/IL-17 Axis.Journal of inflammation research · 2026Article
- A Natural Composite Extract Restores Skin Barrier Function by Modulating Inflammatory, Hydration, and Redox Pathways.Journal of cosmetic dermatology · 2025Article
- Integration of Amazonian resources and curcumin into Jamamina for sustainable nanomaterial development.Scientific reports · 2025Article
- LZTR1 regulates epithelial MHC-I expression via NF-κB1 to modulate CD8Cell discovery · 2025Article
- Review
- CD93 in Health and Disease: Bridging Physiological Functions and Clinical Applications.International journal of molecular sciences · 2025Review
- Interleukin-17D Attenuates OVA-induced Airway Inflammation and Remodeling Partially via the CD93 Receptor.Allergy, asthma & immunology research · 2025Article
- The cytokine CSBF inhibits the IL-17A and TNF-α inflammatory pathways via SUSD2-ACT1 in keratinocytes and alleviates IMQ-induced psoriasis.Cellular & molecular immunology · 2025Article
- The biological activity and potential of probiotics-derived extracellular vesicles as postbiotics in modulating microbiota-host communication.Journal of nanobiotechnology · 2025Review
- IL-17 Ligand and Receptor Family Members Are Differentially Expressed by Keratinocyte Subpopulations and Modulate Their Differentiation and Inflammatory Phenotype.International journal of molecular sciences · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
23 authors.
Xinhui Ni *Shanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.ORCID http://orcid.org/0000-0002-8786-3460
Yi Xu *Shanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.ORCID http://orcid.org/0000-0001-9297-095X
Wang Wang *Shanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.ORCID http://orcid.org/0000-0002-5549-2706
Baida KongShanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.ORCID http://orcid.org/0000-0001-6912-0463
Jian OuyangShanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.ORCID http://orcid.org/0000-0002-7851-7064
Jiwei ChenShanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.
Man YanShanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.
Yawei WuShanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.
Qi ChenShanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.
Xinxin WangShanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.ORCID http://orcid.org/0000-0002-7341-9780
Hongquan LiShanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.
Xiaoguang GaoShanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.ORCID http://orcid.org/0000-0002-8618-9128
Hongquan GuoShanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.ORCID http://orcid.org/0000-0002-1545-8087
Lian CuiDepartment of Dermatology, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.ORCID http://orcid.org/0000-0003-0997-6424
Zeyu ChenDepartment of Dermatology, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.ORCID http://orcid.org/0000-0001-6393-1986
Yuling ShiDepartment of Dermatology, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
Ronghui ZhuDepartment of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.
Wei LiDepartment of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0003-1186-8609
Tieliu ShiShanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.
Lin-Fa WangEmerging Infectious Diseases Program, Duke-NUS Graduate Medical School, Singapore, Singapore.
Jinling HuangInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
Chen DongInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.ORCID http://orcid.org/0000-0002-0084-9130
Yuping LaiShanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China. yplai@bio.ecnu.edu.cn.ORCID http://orcid.org/0000-0001-7445-6738
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant RNA splicing in keratinocytes drives inflammatory skin disorders. In the present study, we found that the RNA helicase DDX5 was downregulated in keratinocytes from the inflammatory skin lesions in patients with atopic dermatitis and psoriasis, and that mice with keratinocyte-specific deletion of Ddx5 (Ddx5
Indexed as
Dermatitis, AtopicInterleukin-27PsoriasisAnimalsInflammationKeratinocytesMiceSkinInterleukin-27
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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.