ArticleCell death & disease2023
TLR7-MyD88-DC-CXCL16 axis results neutrophil activation to elicit inflammatory response in pustular psoriasis.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 22 citations in OpenAlex.
- Keratinocyte-specific STAT3 knockout attenuates imiquimod-induced psoriasiform phenotype in mice.Experimental animals · 2026Article
- Prevotella copri Exacerbates Psoriasis Through Keratinocyte-Neutrophil Crosstalk via NF-κB Activation.Experimental dermatology · 2026Article
- MyD88 Deficiency Protects Mice From Experimental Autoimmune Encephalomyelitis by Influencing Both Dendritic Cells and T Cells.Immunology · 2026Article
- A review of core immuno-inflammatory mechanisms and key regulatory targets in psoriasis.American journal of clinical and experimental immunology · 2026Review
- The active immune role of keratinocytes: from passive targets to key hubs in psoriatic inflammation.Frontiers in immunology · 2026Review
- Comprehensive Metabolomic Profiling of Skin Lesions from Psoriasis Patients Reveals Disease Signatures.International journal of biological sciences · 2026Article
- Advancements in understanding and treating CXCL16/CXCR6 in tumors and in inflammatory diseases: a narrative review.Frontiers in immunology · 2026Review
- From apremilast to JAK inhibitors-salvage treatment strategies for refractory palmoplantar pustulosis: case series.Frontiers in medicine · 2026Article
- Polypeptide sono-adjuvant for ultrasound-activatable regulation of innate immunity and cancer vaccination therapy.Nature communications · 2025Article
- METTL3/ALKBH5-Mediated N6-Methyladenosine Modification Drives Macrophage M1 Polarization via the SLC15A3-TASL-IRF5 Signaling Axis in Psoriasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- MyD88 Signaling in Sertoli Cells Mediates LPS-Induced Orchitis in Mice.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- CXCL16 knockout inhibit asthma airway inflammation by suppressing H2-DM molecular mediated antigen presentation.Cell death discovery · 2025Article
- Review
- Neutrophil extracellular traps in sepsis: trade-off between pros and cons.Burns & trauma · 2025Review
- Sex bias in tumor immunity: insights from immune cells.Theranostics · 2025Review
- Paeoniflorin Attenuates Cognitive Dysfunction and Neuroinflammation by Autophagy in Mice with SLE Induced by Imiquimod.Journal of inflammation research · 2025Article
- Exploring the Role of Chemokine-Related Gene Deregulation and Immune Infiltration in Ischemic Stroke: Insights into CXCL16 and SEMA3E as Potential Biomarkers.Journal of molecular neuroscience : MN · 2024Article
- Chlojaponilactone B Attenuates THP-1 Macrophage Pyroptosis by Inhibiting the TLR/MyD88/NF-κB Pathway.Pharmaceuticals (Basel, Switzerland) · 2024Article
- MDSC-derived S100A8/9 contributes to lupus pathogenesis by promoting TLR7-mediated activation of macrophages and dendritic cells.Cellular and molecular life sciences : CMLS · 2024Article
- Sphingosine 1-phosphate receptor 2 in keratinocytes plays a key role in reducing inflammation in psoriasis.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pustular psoriasis (PP) is a chronic inflammatory disease associated with multiple complications, often with hyperthermia and hypoproteinemia, and its continued progression can be life-threatening. Toll-like receptor 7 (TLR7) induces dendritic cell (DC) production of inflammatory factors that exacerbate the inflammatory response in PP. A membrane-bound chemokine expressed on DCs, CXC motif chemokine ligand 16 (CXCL16) is overexpressed in PP lesions, and neutrophils express its receptor CXC chemokine receptor 6 (CXCR6). There are few studies on the PP immune microenvironment and it is unclear whether TLR7 and CXCL16 can be used as targets in PP therapy. Skin tissue (n = 5) and blood (n = 20) samples were collected from PP and healthy normal controls. The skin tissue transcriptome was analyzed to obtain the differentially expressed genes, and the immune microenvironment was deciphered using pathway enrichment. Tissue sequencing analysis indicated that TLR7, CXCL16, DCs, and neutrophils were involved in the PP process. The enzyme-linked immunosorbent assay, reverse transcription-PCR, and scoring table results demonstrated that TLR7 induced DC secretion of CXCL16, which enabled neutrophil activation of the secretion of the inflammatory factors interleukin-8 (IL-8) and tumor necrosis factor alpha (TNF-α). The co-culture of neutrophils with DCs treated with TLR7 inhibitor or TLR7 agonist demonstrated that TLR7 regulated neutrophil activation, migration, and apoptosis. We constructed imiquimod-induced psoriasis-like skin lesions in wild-type, Cd11c-Cre Myd88
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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.