ArticleScientific reports2018
Granzyme B is elevated in autoimmune blistering diseases and cleaves key anchoring proteins of the dermal-epidermal junction.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 63 citations in OpenAlex.
- T Cell Response Toward Tissue-and Epidermal-Transglutaminases in Coeliac Disease Patients Developing Dermatitis Herpetiformis.Frontiers in immunology · 2021Trial
- Cytotoxic T Cell-Derived Granzyme B Is Increased in SevereFrontiers in immunology · 2019Trial
- Tissue Levels of MMP-9 and Granzyme B in Patients With Bullous Pemphigoid: A Case-Control Study.International journal of dermatology · 2026Article
- Machine learning-based integration develops a novel lysosome-related prognostic signature associated with prognosis and immune infiltration landscape in acute myeloid leukemia.Discover oncology · 2026Article
- Hemidesmosome Mutations Contribute to the Onset and Severity of Acquired Autoimmune Bullous Diseases.MedComm · 2026Article
- Single cell transcriptome profiling reveals pathogenesis of bullous pemphigoid.Communications biology · 2025Article
- Granzyme B cleaves tenascin-C to release its C-terminal domain in rheumatoid arthritis.JCI insight · 2024Article
- Granzyme serine proteases in inflammation and rheumatic diseases.Nature reviews. Rheumatology · 2024Review
- Potential implications of granzyme B in keloids and hypertrophic scars through extracellular matrix remodeling and latent TGF-β activation.Frontiers in immunology · 2024Article
- Integrating Osteopathic Principles for Enhanced Dermatological Outcomes: A Literature Review.Cureus · 2024Review
- Unraveling the Immunopathological Landscape of Celiac Disease: A Comprehensive Review.International journal of molecular sciences · 2023Review
- Granzyme B in Autoimmune Skin Disease.Biomolecules · 2023Review
- In vivo bioluminescence imaging of granzyme B activity in tumor response to cancer immunotherapy.Cell chemical biology · 2022Article
- Etiopathogenesis of dermatitis herpetiformis.Postepy dermatologii i alergologii · 2022Review
- Clinical and immunological characteristics of TGM3 in pan-cancer: A potential prognostic biomarker.Frontiers in genetics · 2022Article
- Potential role of extracellular granzyme B in wet age-related macular degeneration and fuchs endothelial corneal dystrophy.Frontiers in pharmacology · 2022Review
- Granzyme B Induces IRF-3 Phosphorylation through a Perforin-Independent Proteolysis-Dependent Signaling Cascade without Inducing Cell Death.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Association of GZMB polymorphisms and susceptibility to non-segmental vitiligo in a Korean population.Scientific reports · 2021Article
- Granzyme B: a double-edged sword in the response to influenza infection in vaccinated older adults.Frontiers in aging · 2021Article
- Extracellular Matrix Injury of Kidney Allografts in Antibody-Mediated Rejection: A Proteomics Study.Journal of the American Society of Nephrology : JASN · 2020Article
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Authors and funding
18 authors at 4 institutions in 2 countries.
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Abstract
In healthy skin, epidermis and dermis are anchored together at the dermal-epidermal junction (DEJ), a specialized basement membrane pivotal for skin integrity and function. However, increased inflammation in the DEJ is associated with the disruption and separation of this junction and sub-epidermal blistering. Granzyme B (GzmB) is a serine protease secreted by immune cells. Dysregulated inflammation may lead to increased GzmB accumulation and proteolysis in the extracellular milieu. Although elevated GzmB is observed at the level of the DEJ in inflammatory and blistering skin conditions, the present study is the first to explore GzmB in the context of DEJ degradation in autoimmune sub-epidermal blistering. In the present study, GzmB induced separation of the DEJ in healthy human skin. Subsequently, α6/β4 integrin, collagen VII, and collagen XVII were identified as extracellular substrates for GzmB through western blot, and specific cleavage sites were identified by mass spectrometry. In human bullous pemphigoid, dermatitis herpetiformis, and epidermolysis bullosa acquisita, GzmB was elevated at the DEJ when compared to healthy samples, while α6/β4 integrin, collagen VII, and collagen XVII were reduced or absent in the area of blistering. In summary, our results suggest that regardless of the initial causation of sub-epidermal blistering, GzmB activity is a common final pathway that could be amenable to a single targeted treatment approach.
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