ArticleJournal of the American Society of Nephrology : JASN2016
Myeloperoxidase Peptide-Based Nasal Tolerance in Experimental ANCA-Associated GN.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Can we cure vasculitis?Current opinion in immunology · 2025Review
- Mechanisms of vascular damage in ANCA vasculitis.Seminars in immunopathology · 2022Review
- Restricted myeloperoxidase epitopes drive the adaptive immune response in MPO-ANCA vasculitis.Journal of autoimmunity · 2020Article
- Animal Models of ANCA Associated Vasculitis.Frontiers in immunology · 2020Review
- Tolerogenic Dendritic Cells Attenuate Experimental Autoimmune Antimyeloperoxidase Glomerulonephritis.Journal of the American Society of Nephrology : JASN · 2019Article
- T-lymphocyte in ANCA-associated vasculitis: what do we know? A pathophysiological and therapeutic approach.Clinical kidney journal · 2019Article
- Apoptotic Cell-Induced, Antigen-Specific Immunoregulation to Treat Experimental Antimyeloperoxidase GN.Journal of the American Society of Nephrology : JASN · 2019Article
- Regulatory T cells in renal disease.Clinical & translational immunology · 2018Review
- CD8+ T Cells Effect Glomerular Injury in Experimental Anti-Myeloperoxidase GN.Journal of the American Society of Nephrology : JASN · 2017Article
- Disentangling the role of neutrophil extracellular traps in rheumatic diseases.Current opinion in rheumatology · 2017Review
- Immune Response against Autoantigen PLA2R Is not Gambling: Implications for Pathophysiology, Prognosis, and Therapy.Journal of the American Society of Nephrology : JASN · 2016Article
- Overview of the Pathogenesis of ANCA-Associated Vasculitis.Kidney diseases (Basel, Switzerland) · 2016Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Less toxic treatment options for patients with myeloperoxidase (MPO)-ANCA-associated GN are needed. Using an established murine model of focal necrotizing GN mediated by autoimmunity to MPO (autoimmune anti-MPO GN), we assessed the capacity for nasal tolerance induced by nasal insufflation of the immunodominant nephritogenic MPO peptide (MPO409-428) to attenuate this disease. Compared with mice that received an irrelevant immunodominant ovalbumin (OVA) peptide, OVA323-339, mice that received MPO409-428 were protected from the development of humoral and cell-mediated autoimmunity to full-length MPO and the development of GN. In mice with established anti-MPO autoimmunity, nasal insufflation of MPO409-428 as a therapeutic attenuated anti-MPO GN. To investigate the nature of this induced tolerance, we isolated CD4(+) T cells from the upper airway draining lymph nodes of both OVA323-339- and MPO409-428-tolerized mice. Adoptive transfer of CD4(+) T cells from MPO409-428- but not OVA323-339-tolerized mice to animals with established anti-MPO autoimmunity attenuated the subsequent development of GN, confirming that the immunosuppression induced by these T cells is antigen specific. Ex vivo studies showed that nasal tolerance to MPO is mediated by both conventional and induced T regulatory cells. The strong homology between the pathogenic human MPO B cell epitope recognized by ANCA in patients with acute vasculitis and the nephritogenic murine T cell MPO epitope emphasizes the clinical relevance of this study.
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