ArticleFrontiers in immunology2022
Anti-FcαRI Monoclonal Antibodies Resolve IgA Autoantibody-Mediated Disease.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Construction of LncRNA-miRNA-mRNA regulatory network in IgA nephropathy mice model by RNA-sequencing and bioinformatics analysis.Genes & genomics · 2025Article
- Biomarker understanding first lessons from drug development for IgA-driven autoimmune and fibrotic diseases.Cambridge prisms. Precision medicine · 2025Review
- Neutrophil extracellular traps and interleukin-1β in cystic fibrosis lung disease.Frontiers in immunology · 2025Review
- Article
- Anti-NC16A IgA from Patients with Linear IgA Bullous Dermatosis Induce Neutrophil-Dependent Subepidermal Blistering in Mice.The Journal of investigative dermatology · 2024Article
- Linear IgA bullous dermatosis-a fifty year experience of Warsaw Center of bullous diseases.Frontiers in immunology · 2024Review
- Antagonizing FcαR1 (CD89) as treatment in IgA-mediated chronic inflammation and autoimmunity.Frontiers in immunology · 2023Article
- IgA-producing B cells in lung homeostasis and disease.Frontiers in immunology · 2023Review
- Fcα Receptor-1-Activated Monocytes Promote B Lymphocyte Migration and IgA Isotype Switching.International journal of molecular sciences · 2022Article
- Current knowledge of targeted-release budesonide in immunoglobulin A nephropathy: A comprehensive review.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoglobulin A (IgA) is generally considered as a non-inflammatory regulator of mucosal immunity, and its importance in diversifying the gut microbiota is increasingly appreciated. IgA autoantibodies have been found in several autoimmune or chronic inflammatory diseases, but their role in pathophysiology is ill-understood. IgA can interact with the Fc receptor FcαRI on immune cells. We now established a novel IgA autoimmune blistering model, which closely resembles the human disease linear IgA bullous disease (LABD) by using genetically modified mice that produce human IgA and express human FcαRI. Intravital microscopy demonstrated that presence of IgA anti-collagen XVII, - the auto-antigen in LABD-, resulted in neutrophil activation and extravasation from blood vessels into skin tissue. Continued exposure to anti-collagen XVII IgA led to massive neutrophil accumulation, severe tissue damage and blister formation. Importantly, treatment with anti-FcαRI monoclonal antibodies not only prevented disease, but was also able to resolve existing inflammation and tissue damage. Collectively, our data reveal a novel role of neutrophil FcαRI in IgA autoantibody-mediated disease and identify FcαRI as promising new therapeutic target to resolve chronic inflammation and tissue damage.
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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.