Autoreactive Plasmablasts After B Cell Depletion With Rituximab and Relapses in Antineutrophil Cytoplasmic Antibody-Associated Vasculitis.


Journal

Arthritis & rheumatology (Hoboken, N.J.)
ISSN: 2326-5205
Titre abrégé: Arthritis Rheumatol
Pays: United States
ID NLM: 101623795

Informations de publication

Date de publication:
05 2023
Historique:
revised: 04 09 2022
received: 24 07 2021
accepted: 11 10 2022
pmc-release: 01 05 2024
medline: 17 5 2023
pubmed: 26 10 2022
entrez: 25 10 2022
Statut: ppublish

Résumé

Autoreactive B cells are responsible for antineutrophil cytoplasmic antibody (ANCA) production in ANCA-associated vasculitis (AAV). Rituximab (RTX) depletes circulating B cells, including autoreactive B cells. We aimed to evaluate changes and associations with relapse of the circulating autoreactive B cell pool following therapeutic B cell depletion in AAV. Sequential flow cytometry was performed on 148 samples of peripheral blood mononuclear cells from 23 patients with proteinase 3 (PR3)-ANCA-positive AAV who were treated with RTX for remission induction and monitored after stopping therapy during long-term follow-up in a prospective clinical trial. PR3 was used as a ligand to target autoreactive PR3-specific (PR3+) B cells. B cell recurrence was considered as the first blood sample with ≥10 B cells/μl after RTX treatment. At B cell recurrence, PR3+ B cell frequency among B cells was higher than baseline (P < 0.01). Within both PR3+ and total B cells, frequencies of transitional and naive subsets were higher at B cell recurrence than at baseline, while memory subsets were lower (P < 0.001 for all comparisons). At B cell recurrence, frequencies of B cells and subsets did not differ between patients who experienced relapse and patients who remained in remission. In contrast, the plasmablast frequency within the PR3+ B cell pool was higher in patients who experienced relapse and associated with a shorter time to relapse. Frequencies of PR3+ plasmablasts higher than baseline were more likely to be found in patients who experienced relapse within the following 12 months compared to those in sustained remission (P < 0.05). The composition of the autoreactive B cell pool varies significantly following RTX treatment in AAV, and early plasmablast enrichment within the autoreactive pool is associated with future relapses.

Identifiants

pubmed: 36281741
doi: 10.1002/art.42388
pmc: PMC10280646
mid: NIHMS1844052
doi:

Substances chimiques

Rituximab 4F4X42SYQ6
Antibodies, Antineutrophil Cytoplasmic 0
Myeloblastin EC 3.4.21.76

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

736-747

Subventions

Organisme : NIAID NIH HHS
ID : N01AI15416
Pays : United States
Organisme : NIAMS NIH HHS
ID : RC1 AR058303
Pays : United States
Organisme : NIAID NIH HHS
ID : UM1 AI109565
Pays : United States

Informations de copyright

© 2022 The Authors. Arthritis & Rheumatology published by Wiley Periodicals LLC on behalf of American College of Rheumatology.

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Auteurs

Alvise Berti (A)

Division of Pulmonary & Critical Care Medicine, Thoracic Disease Research Unit, Mayo Clinic, Rochester, Minnesota, and Center for Medical Sciences (CISMed), Department of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, Italy, and Rheumatology Unit, Santa Chiara Hospital, APSS Trento, Italy.

Sophie Hillion (S)

Université de Bretagne Occidendale, Brest, Bretagne, France.

Maximilian F Konig (MF)

Division of Rheumatology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland.

Marta Casal Moura (MC)

Division of Pulmonary & Critical Care Medicine, Thoracic Disease Research Unit, Mayo Clinic, Rochester, Minnesota.

Amber M Hummel (AM)

Division of Pulmonary & Critical Care Medicine, Thoracic Disease Research Unit, Mayo Clinic, Rochester, Minnesota.

Eva Carmona (E)

Division of Pulmonary & Critical Care Medicine, Thoracic Disease Research Unit, Mayo Clinic, Rochester, Minnesota.

Tobias Peikert (T)

Division of Pulmonary & Critical Care Medicine, Thoracic Disease Research Unit, Mayo Clinic, Rochester, Minnesota.

Fernando C Fervenza (FC)

Division of Nephrology & Hypertension, Mayo Clinic, Rochester, Minnesota.

Cees G M Kallenberg (CGM)

Department of Rheumatology and Clinical Immunology, University of Groningen, Groningen, The Netherlands.

Carol A Langford (CA)

Cleveland Clinic, Cleveland, Ohio.

Peter A Merkel (PA)

Division of Rheumatology, Department of Medicine, and Department of Biostatistics, Epidemiology, and Informatics, Division of Clinical Epidemiology, University of Pennsylvania, Philadelphia.

Paul A Monach (PA)

Brigham and Women's Hospital, Boston, Massachusetts.

Philip Seo (P)

Division of Rheumatology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland.

Robert F Spiera (RF)

Weill Cornell Medical College, Hospital for Special Surgery, New York.

Paul Brunetta (P)

Genentech, Inc, San Francisco, California.

E William St Clair (EW)

Duke University, Durham, North Carolina.

Kristina M Harris (KM)

Immune Tolerance Network, Bethesda, Maryland.

John H Stone (JH)

Massachusetts General Hospital Rheumatology Unit, Boston.

Guido Grandi (G)

Department of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, Italy.

Jacques-Olivier Pers (JO)

Université de Bretagne Occidendale, Brest, Bretagne, France.

Ulrich Specks (U)

Division of Pulmonary & Critical Care Medicine, Thoracic Disease Research Unit, Mayo Clinic, Rochester, Minnesota.

Divi Cornec (D)

Université de Bretagne Occidendale, Brest, Bretagne, France.

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Classifications MeSH