ArticleThe Journal of investigative dermatology2017
The Syk Tyrosine Kinase Is Required for Skin Inflammation in an In Vivo Mouse Model of Epidermolysis Bullosa Acquisita.
Article in The Journal of investigative dermatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- The Src-Family Kinases Hck, Fgr and Lyn Drive Immune Complex-Mediated Glomerulonephritis Through the Syk Tyrosine Kinase.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Tyrosine kinase signaling pathways as therapeutic targets in autoimmune subepidermal blistering skin diseases (pemphigoid diseases).Frontiers in immunology · 2026Review
- Pemphigoid disease model systems for clinical translation.Frontiers in immunology · 2025Review
- Tyrosine Protein Kinase SYK-Related Gene Signature in Baseline Immune Cells Associated with Adjuvant Immunotherapy-Induced Immune-Related Adverse Events in Melanoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Myeloid Src-family kinases are critical for neutrophil-mediated autoinflammation in gout and motheaten models.The Journal of experimental medicine · 2023Article
- New small molecules in dermatology: for the autoimmunity, inflammation and beyond.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- The selective inhibition of the Syk tyrosine kinase ameliorates experimental autoimmune arthritis.Frontiers in immunology · 2023Article
- Monocyte populations are involved in the pathogenesis of experimental epidermolysis bullosa acquisita.Frontiers in immunology · 2023Article
- Amelioration of Lupus Serum-Induced Skin Inflammation in CD64-Deficient Mice.Frontiers in immunology · 2022Article
- Cutaneous kinase activity correlates with treatment outcomes following PI3K delta inhibition in mice with experimental pemphigoid diseases.Frontiers in immunology · 2022Article
- Spleen tyrosine kinase facilitates neutrophil activation and worsens long-term neurologic deficits after spinal cord injury.Journal of neuroinflammation · 2021Article
- miR-136 improves renal fibrosis in diabetic rats by targeting down-regulation of tyrosine kinase SYK and inhibition of TGF-β1/Smad3 signaling pathway.Renal failure · 2020Article
- Caffeoyl-Prolyl-Histidine Amide Inhibits Fyn and Alleviates Atopic Dermatitis-Like Phenotypes via Suppression of NF-κB Activation.International journal of molecular sciences · 2020Article
- Neutrophils as emerging therapeutic targets.Nature reviews. Drug discovery · 2020Review
- Drug Development in Pemphigoid Diseases.Acta dermato-venereologica · 2020Review
- Tyrosine Kinases in Autoimmune and Inflammatory Skin Diseases.Frontiers in immunology · 2019Review
- Hematopoietic or Osteoclast-Specific Deletion of Syk Leads to Increased Bone Mass in Experimental Mice.Frontiers in immunology · 2019Article
- Editorial: Autoantibodies.Frontiers in immunology · 2019Article
- Myeloid-Specific Deletion of Mcl-1 Yields Severely Neutropenic Mice That Survive and Breed in Homozygous Form.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Whole-Genome Expression Profiling in Skin Reveals SYK As a Key Regulator of Inflammation in Experimental Epidermolysis Bullosa Acquisita.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inflammatory form of epidermolysis bullosa acquisita is caused by autoantibodies against type VII collagen (C7), a component of the dermal-epidermal junction. We have previously shown that myeloid Src family kinases mediate skin inflammation triggered by anti-C7 antibodies. Here we identify the Syk tyrosine kinase as a critical component of autoantibody-induced skin inflammation downstream of Src family kinases. Immobilized C7-anti-C7 immune complexes triggered neutrophil activation and Syk phosphorylation in a Src family kinase-dependent manner. Bone marrow chimeric mice lacking Syk in their hematopoietic compartment were completely protected from skin inflammation triggered by anti-C7 antibodies despite normal circulating anti-C7 levels. Syk deficiency abrogated the accumulation of CXCL2, IL-1β, and leukotriene B
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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.