ArticleScientific reports2016
T cells mediate autoantibody-induced cutaneous inflammation and blistering in epidermolysis bullosa acquisita.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 47 citations in OpenAlex.
- CDK7, CDK9, or CDK11 inhibition reduces neutrophil-driven inflammation and tissue damage in experimental autoimmune models.Cell communication and signaling : CCS · 2026Article
- CD19×CD3 bispecific T cell engager treatment induces remission in experimental pemphigoid disease.Molecular therapy. Advances · 2026Article
- Pemphigoid disease model systems for clinical translation.Frontiers in immunology · 2025Review
- Rituximab in the Management of Autoimmune Bullous Diseases: A Treatment-Resistant Case Series from a Single Central European Referral Center.Medicina (Kaunas, Lithuania) · 2024Article
- Inhibition of interferon gamma impairs induction of experimental epidermolysis bullosa acquisita.Frontiers in immunology · 2024Article
- The complement receptor C5aR2 regulates neutrophil activation and function contributing to neutrophil-driven epidermolysis bullosa acquisita.Frontiers in immunology · 2023Article
- C-type lectin receptor expression is a hallmark of neutrophils infiltrating the skin in epidermolysis bullosa acquisita.Frontiers in immunology · 2023Article
- Human skin dermis-derived fibroblasts are a kind of functional mesenchymal stromal cells: judgements from surface markers, biological characteristics, to therapeutic efficacy.Cell & bioscience · 2022Article
- Therapeutic effects of Fc gamma RIV inhibition are mediated by selectively blocking immune complex-induced neutrophil activation in epidermolysis bullosa acquisita.Frontiers in immunology · 2022Article
- A Review of Acquired Autoimmune Blistering Diseases in Inherited Epidermolysis Bullosa: Implications for the Future of Gene Therapy.Antibodies (Basel, Switzerland) · 2021Review
- Preventive but Not Therapeutic Topical Application of Local Anesthetics Can Inhibit Experimental Epidermolysis Bullosa Acquisita in Mice.Frontiers in immunology · 2021Article
- Topical Application of the PI3Kβ-Selective Small Molecule Inhibitor TGX-221 Is an Effective Treatment Option for Experimental Epidermolysis Bullosa Acquisita.Frontiers in medicine · 2021Article
- Treatment with anti-neonatal Fc receptor (FcRn) antibody ameliorates experimental epidermolysis bullosa acquisita in mice.British journal of pharmacology · 2020Article
- The G Protein-Coupled Receptor (GPR) 15 Counteracts Antibody-Mediated Skin Inflammation.Frontiers in immunology · 2020Article
- Skin Barrier and Autoimmunity-Mechanisms and Novel Therapeutic Approaches for Autoimmune Blistering Diseases of the Skin.Frontiers in immunology · 2019Review
- Fcγ Receptor IIB Controls Skin Inflammation in an Active Model of Epidermolysis Bullosa Acquisita.Frontiers in immunology · 2019Article
- Unraveling the ECM-Immune Cell Crosstalk in Skin Diseases.Frontiers in cell and developmental biology · 2019Review
- Epidermolysis Bullosa Acquisita: The 2019 Update.Frontiers in medicine · 2018Review
- Whole-Genome Expression Profiling in Skin Reveals SYK As a Key Regulator of Inflammation in Experimental Epidermolysis Bullosa Acquisita.Frontiers in immunology · 2018Article
- The Immunometabolomic Interface Receptor Hydroxycarboxylic Acid Receptor 2 Mediates the Therapeutic Effects of Dimethyl Fumarate in Autoantibody-Induced Skin Inflammation.Frontiers in immunology · 2018Article
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cells are key players in autoimmune diseases by supporting the production of autoantibodies. However, their contribution to the effector phase of antibody-mediated autoimmune dermatoses, i.e., tissue injury and inflammation of the skin, has not been investigated. In this paper, we demonstrate that T cells amplify the development of autoantibody-induced tissue injury in a prototypical, organ-specific autoimmune disease, namely epidermolysis bullosa acquisita (EBA) - characterized and caused by autoantibodies targeting type VII collagen. Specifically, we show that immune complex (IC)-induced inflammation depends on the presence of T cells - a process facilitated by T cell receptor (TCR)γδ and NKT cells. Because tissue damage in IC-induced inflammation is neutrophil-dependent, we further analyze the interplay between T cells and neutrophils in an experimental model of EBA. We demonstrate that T cells not only enhance neutrophil recruitment into the site of inflammation but also interact with neutrophils in lymphatic organs. Collectively, this study shows that T cells amplify the effector phase of antibody-induced tissue inflammation.
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