ArticleThe American journal of pathology2013
Bullous pemphigoid IgG induces BP180 internalization via a macropinocytic pathway.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 64 citations in OpenAlex.
- Hemidesmosome Mutations Contribute to the Onset and Severity of Acquired Autoimmune Bullous Diseases.MedComm · 2026Article
- IgG autoantibodies in bullous pemphigoid induce a pathogenic MyD88-dependent pro-inflammatory response in keratinocytes.Nature communications · 2025Article
- Autoimmune bullous diseases: pathogenesis and clinical management.Molecular biomedicine · 2025Review
- Bullous pemphigoid.Nature reviews. Disease primers · 2025Review
- Pemphigoid disease model systems for clinical translation.Frontiers in immunology · 2025Review
- From Molecular Insights to Clinical Perspectives in Drug-Associated Bullous Pemphigoid.International journal of molecular sciences · 2023Review
- Extracellular matrix in skin diseases: The road to new therapies.Journal of advanced research · 2023Review
- Pruritogens in pemphigoid diseases: Possible therapeutic targets for a burdensome symptom.The Journal of dermatology · 2023Review
- Targeting type 2 inflammation in bullous pemphigoid: current and emerging therapeutic approaches.Frontiers in medicine · 2023Review
- Adaptive and innate immune pathogenesis of bullous pemphigoid: A review.Frontiers in immunology · 2023Review
- Insights Into the Pathogenesis of Bullous Pemphigoid: The Role of Complement-Independent Mechanisms.Frontiers in immunology · 2022Review
- Interleukin-26-DNA complexes promote inflammation and dermal-epidermal separation in a modified human cryosection model of bullous pemphigoid.Frontiers in immunology · 2022Article
- The relevance of complement in pemphigoid diseases: A critical appraisal.Frontiers in immunology · 2022Review
- Type XVII collagen: Relevance of distinct epitopes, complement-independent effects, and association with neurological disorders in pemphigoid disorders.Frontiers in immunology · 2022Review
- BP180/Collagen XVII: A Molecular View.International journal of molecular sciences · 2021Review
- Granzyme B inhibition reduces disease severity in autoimmune blistering diseases.Nature communications · 2021Article
- Subunit-Specific Reactivity of Autoantibodies Against Laminin-332 Reveals Direct Inflammatory Mechanisms on Keratinocytes.Frontiers in immunology · 2021Article
- Presence of Cutaneous Complement Deposition Distinguishes between Immunological and Histological Features of Bullous Pemphigoid-Insights from a Retrospective Cohort Study.Journal of clinical medicine · 2020Article
- Intracellular accumulation of PD-1 molecules in circulating T lymphocytes in advanced malignant melanoma: an implication for immune evasion mechanism.International journal of clinical oncology · 2020Article
- Adenovirus-Mediated LAMA3 Transduction Enhances Hemidesmosome Formation and Periodontal Reattachment during Wound Healing.Molecular therapy. Methods & clinical development · 2020Article
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Authors and funding
9 authors at 5 institutions in 2 countries.
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Abstract
Bullous pemphigoid (BP) is an autoimmune blistering skin disease induced by pathogenic autoantibodies against a type II transmembrane protein (BP180, collagen type XVII, or BPAG2). In animal models, BP180 autoantibody-antigen interaction appears insufficient to develop blisters, but involvement of complement and neutrophils is required. However, cultured keratinocytes treated with BP-IgG exhibit a reduction in the adhesive strength and a loss of expression of BP180, suggesting that the autoantibodies directly affect epidermal cell-extracellular matrix integrity. In this study, we explored the consequences of two distinct epithelial cells treated with BP-IgG, particularly the fate of BP180. First, we followed the distribution of green fluorescent protein-tagged BP180 in an epithelial cell line, 804G, and normal human epidermal keratinocytes after autoantibody clustering. After BP-IgG treatment, the adhesive strength of the cells to their substrate was decreased, and BP180 was internalized in both cell types, together with the early endosomal antigen-1. By using various endocytosis inhibitors and a fluid-uptake assay, we demonstrated that BP-IgG-induced BP180 internalization is mediated via a macropinocytic pathway. Moreover, a macropinocytosis inhibitor rescued a BP-IgG-induced reduction in the adhesive strength of the cells from their substrate. The results of this study suggest that BP180 internalization induced by BP-IgG plays an important role in the initiation of disease pathogenesis.
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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.