ArticleThe Journal of clinical investigation2006
Pathogenic role for skin macrophages in a mouse model of keratinocyte-induced psoriasis-like skin inflammation.
Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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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.
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Who cites it
82 citing papers in PubMed, 211 citations in OpenAlex.
- Targeting Cannabinoid 1 Receptor in Macrophages Alleviates Psoriatic Skin Inflammation Through the AUF1-NLRP3 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Bcl-3 expression in the imiquimod-induced psoriasis mouse skin.BMC research notes · 2026Article
- Galectin-1 deficiency attenuates imiquimod-induced psoriasiform skin inflammation and is associated with reduced macrophage recruitment.Frontiers in immunology · 2026Article
- Jaungo-based herbal complex regulates psoriasis-associated macrophage-keratinocyte inflammatory axis.Frontiers in pharmacology · 2026Article
- Advances in Psoriasis Research: Decoding Immune Circuits and Developing Novel Therapies.International journal of molecular sciences · 2025Review
- Quercetin mediates the therapeutic effect ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Skin immunity and inflammation: cellular interactions and communication.Clinical & translational immunology · 2025Review
- Review: A Contemporary, Multifaced Insight into Psoriasis Pathogenesis.Journal of personalized medicine · 2024Review
- Macrophage Functions in Psoriasis: Lessons from Mouse Models.International journal of molecular sciences · 2024Review
- The Immunology of Psoriasis-Current Concepts in Pathogenesis.Clinical reviews in allergy & immunology · 2024Review
- A co-assembly platform engaging macrophage scavenger receptor A for lysosome-targeting protein degradation.Nature communications · 2024Article
- Exploration of ferroptosis and necroptosis-related genes and potential molecular mechanisms in psoriasis and atherosclerosis.Frontiers in immunology · 2024Article
- Tick cysteine protease inhibitors suppress immune responses in mannan-induced psoriasis-like inflammation.Frontiers in immunology · 2024Article
- Macrophages mediate psoriasis via Mincle-dependent mechanism in mice.Cell death discovery · 2023Article
- Resveratrol Ameliorates Imiquimod-Induced Psoriasis-Like Mouse Model via Reducing Macrophage Infiltration and Inhibiting Glycolysis.Journal of inflammation research · 2023Article
- The integration of large-scale public data and network analysis uncovers molecular characteristics of psoriasis.Human genomics · 2022Article
- Macrophages in Skin Wounds: Functions and Therapeutic Potential.Biomolecules · 2022Review
- Mouse Models of Psoriasis: A Comprehensive Review.The Journal of investigative dermatology · 2022Review
- Psoriasiform Inflammation Is Associated with Mitochondrial Fission/GDAP1L1 Signaling in Macrophages.International journal of molecular sciences · 2021Article
- The RNase MCPIP3 promotes skin inflammation by orchestrating myeloid cytokine response.Nature communications · 2021Article
22 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is a common skin disease, the pathogenesis of which has not yet been resolved. In mice, epidermis-specific deletion of inhibitor of NF-kappaB (IkappaB) kinase 2 (IKK2) results in a skin phenotype that mimics human psoriasis in several aspects. Like psoriasis, this skin disease shows pronounced improvement when mice are treated with a TNF-neutralizing agent. We have found previously that this phenotype does not depend on the presence of alphabeta T lymphocytes. In order to evaluate contributions of other immune cell populations to the skin disease, we selectively eliminated macrophages and granulocytes from the skin of mice with epidermis-specific deletion of IKK2 (K14-Cre-IKK2fl/fl mice). Elimination of skin macrophages by subcutaneous injection of clodronate liposomes was accompanied by inhibition of granulocyte migration into the skin and resulted in a dramatic attenuation of psoriasis-like skin changes. The hyperproliferative, inflammatory skin disease in K14-Cre-IKK2fl/fl mice was a direct consequence of the presence of macrophages in the skin, as targeted deletion of CD18, which prevented accumulation of granulocytes but not macrophages, did not lead to major changes in the phenotype. Targeted deletion of the receptor for IFN-gamma revealed that the pathogenesis of the skin disease does not depend on classical IFN-gamma-mediated macrophage activation. Our results demonstrate that in mice epidermal keratinocytes can initiate a hyperproliferative, inflammatory, IFN-gamma-independent, psoriasis-like skin disease whose development requires essential contributions from skin macrophages but not from granulocytes or alphabeta T lymphocytes.
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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.