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Breaking ANCA

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Mucosal Breaks of Bacteria Trigger Pathogenic B-cell Responses in ANCA-associate...

Mucosal Breaks of Bacteria Trigger Pathogenic B-cell Responses in ANCA-associated Vasculitis ANCA-associated vasculitis (AAV) is a rare and severe autoimmune disease, characterized by inflammation of the small blood vessels. ANCAs, autoantibodies against proteinase-3 (PR3) or myeloperoxidase (MPO), play a central role in... ver más

30/04/2027

Leiden University...

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ACADEMISCH ZIEKENHUIS LEIDEN No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo HORIZON EUROPE notifico la concesión del proyecto el día 2024-05-01

HORIZON-MSCA-2023-PF-01-01: MSCA Postdoctoral Fellowships 2023 ExpectedOutcome:Project results are expected to contribute to the following outcomes:

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Leiden University Medical Ce...

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Duración del proyecto: 35 meses Fecha Inicio: 2024-05-01
Fecha Fin: 2027-04-30

Líder del proyecto

ACADEMISCH ZIEKENHUIS LEIDEN No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto ANCA-associated vasculitis (AAV) is a rare and severe autoimmune disease, characterized by inflammation of the small blood vessels. ANCAs, autoantibodies against proteinase-3 (PR3) or myeloperoxidase (MPO), play a central role in the pathogenesis. They induce excessive activation of neutrophils, resulting in necrotizing injury of small vessels. The loss of tolerance in AAV is thought to be the result of genetic, environmental, and ageing factors. Although infectious triggers are implicated, their exact role in the pathogenesis of AAV remains unclear. Previous studies demonstrated that AAV patients with chronic nasal carriage of Staphylococcus aureus or Corynebacterium tuberculostearicum exhibited a higher relapse rate, and eradication treatment reduced relapses. We hypothesize that pathogenic sinonasal mucosal breaks of bacteria activate autoreactive B-cells through molecular mimicry, resulting in autoimmune responses that mediate AAV. This proposal is to investigate the role of sinonasal mucosal breaks in AAV through repertoire sequencing of peripheral blood and tissue B-cells of AAV patients combined with 16S sequencing of the sinonasal bacterial microbiome. Subsequently, representative monoclonal antibodies will be expressed and reactivity towards ANCAs and sinonasal bacterial antigens investigated. Lastly, the findings will be validated by studying serum antibody reactivity in large cohorts of AAV patients. Success of the proposed studies would transform our understanding of the autoimmune responses in AAV, and potentially elucidate a mechanistic role for sinonasal mucosal breaks of bacteria in triggering disease initiation and progression. Further, success could lead to novel therapeutic approaches focused on preventing mucosal breaks and/or clearance of pathogenic strains. Through this fellowship I hope to develop myself into an independent reseacher, expert of AAV and obtain a position as future academic clinician and principal investigator.

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