ArticleExperimental dermatology2012
Collagen XVII (BP180) modulates keratinocyte expression of the proinflammatory chemokine, IL-8.
Article in Experimental dermatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 30 citations in OpenAlex.
- PPP1R14B as a potential biomarker for the identification of diagnosis and prognosis affecting tumor immunity, proliferation and migration in prostate cancer.Journal of Cancer · 2024Article
- Advancing Treatment in Bullous Pemphigoid: A Comprehensive Review of Novel Therapeutic Targets and Approaches.Clinical reviews in allergy & immunology · 2023Review
- Identification of Key Immune-Related Genes in the Treatment of Heart Failure After Myocardial Infarction with Empagliflozin Based on RNA-Seq.Journal of inflammation research · 2023Article
- Gene expression profiling of laminin α3-blocked keratinocytes reveals an immune-independent mechanism of blistering.Experimental dermatology · 2022Article
- Type XVII collagen: Relevance of distinct epitopes, complement-independent effects, and association with neurological disorders in pemphigoid disorders.Frontiers in immunology · 2022Review
- Insights Into the Pathogenesis of Bullous Pemphigoid: The Role of Complement-Independent Mechanisms.Frontiers in immunology · 2022Review
- A Review of Acquired Autoimmune Blistering Diseases in Inherited Epidermolysis Bullosa: Implications for the Future of Gene Therapy.Antibodies (Basel, Switzerland) · 2021Review
- Granzyme B inhibition reduces disease severity in autoimmune blistering diseases.Nature communications · 2021Article
- Non-Cell-Autonomous Activity of the Hemidesmosomal Protein BP180/Collagen XVII in Granulopoiesis in Humanized NC16A Mice.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- The dysfunction of BP180/collagen XVII in keratinocytes promotes melanoma progression.Oncogene · 2019Article
- Proteases in Pemphigoid Diseases.Frontiers in immunology · 2019Review
- The Role of Eosinophils in Bullous Pemphigoid: A Developing Model of Eosinophil Pathogenicity in Mucocutaneous Disease.Frontiers in medicine · 2018Review
- BP180 Is Critical in the Autoimmunity of Bullous Pemphigoid.Frontiers in immunology · 2017Review
- Hsp90 blockade modulates bullous pemphigoid IgG-induced IL-8 production by keratinocytes.Cell stress & chaperones · 2014Article
- Erythrodermic psoriasis with bullous pemphigoid: combination treatment with methotrexate and compound glycyrrhizin.Diagnostic pathology · 2014Article
- Secrets of the cutaneous basement membrane.The Journal of investigative dermatology · 2014Article
- Long-term survival of type XVII collagen revertant cells in an animal model of revertant cell therapy.The Journal of investigative dermatology · 2014Article
- Aberrant expression and secretion of heat shock protein 90 in patients with bullous pemphigoid.PloS one · 2013Article
- Collagen XVII: a shared antigen in neurodermatological interactions?Clinical & developmental immunology · 2013Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Collagen XVII (COL17), a transmembrane protein expressed in epidermal keratinocytes (EK), is targeted by pathogenic autoantibodies in bullous pemphigoid. Treatment of EK with anti-COL17 autoantibodies triggers the production of proinflammatory cytokines. In this study, we test the hypothesis that COL17 is involved in the regulation of the EK proinflammatory response, using IL-8 expression as the primary readout. The absence of COL17 in EK derived from a junctional epidermolysis bullosa patient or shRNA-mediated knockdown of COL17 in normal EK resulted in a dysregulation of IL-8 responses under various conditions. The COL17-deficient cells showed an abnormally high IL-8 response after treatment with lipopolysaccharide (LPS), ultraviolet-B radiation or tumor necrosis factor, but exhibited a blunted IL-8 response to phorbol 12-myristate 13-acetate exposure. Induction of COL17 expression in COL17-negative EK led to a normalization of the LPS-induced proinflammatory response. Although α6β4 integrin was found to be up-regulated in COL17-deficient EK, siRNA-mediated knockdown of the α6 and β4 subunits revealed that COL17's effects on the LPS IL-8 response are not dependent on this integrin. In LPS-treated cells, inhibition of NF-kappa B activity in COL17-negative EK resulted in a normalization of their IL-8 response, and expression of an NF-kappa B-driven reporter was shown to be higher in COL17-deficient, compared with normal EK. These findings support the hypothesis that COL17 plays an important regulatory role in the EK proinflammatory response, acting largely via NF-kappa B. Future investigations will focus on further defining the molecular basis of this novel control network.
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