Anti-C1q Antibodies as Occurring in Systemic Lupus Erythematosus Could Be Induced by an Epstein-Barr Virus-Derived Antigenic Site.


Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2019
Historique:
received: 05 05 2019
accepted: 21 10 2019
entrez: 3 12 2019
pubmed: 4 12 2019
medline: 4 11 2020
Statut: epublish

Résumé

Previous infection with Epstein-Barr virus (EBV) is believed to trigger autoimmunity and to drive autoantibody generation as occurring in patients with systemic lupus erythematosus (SLE). Complement C1q and autoantibodies targeting it (anti-C1q) are also considered to be involved in the pathogenesis of SLE, independently of the impact of environmental insults. Still, the circumstances under which these autoantibodies arise remain elusive. By studying a major antigenic site of C1q targeted by anti-C1q (A08), we aimed to determine environmental factors and possible mechanisms leading to the development of anti-C1q. First, we determined antigenic residues of A08 that were critical for the binding of anti-C1q; importantly, we found the binding to depend on amino-acid-identity. Anti-C1q of SLE patients targeting these critical antigenic residues specifically cross-reacted with the EBV-related EBNA-1 (Epstein-Barr virus nuclear antigen 1)-derived peptide EBNA348. In a cohort of 180 SLE patients we confirmed that patients that were seropositive for EBV and recognized the EBNA348 peptide had increased levels of anti-A08 and anti-C1q, respectively. The correlation of anti-EBNA348 with anti-A08 levels was stronger in SLE patients than in matched healthy controls. Finally, EBNA348 peptide-immunization of C1q

Identifiants

pubmed: 31787984
doi: 10.3389/fimmu.2019.02619
pmc: PMC6853867
doi:

Substances chimiques

Autoantibodies 0
Epstein-Barr Virus Nuclear Antigens 0
Complement C1q 80295-33-6
EBV-encoded nuclear antigen 1 O5GA75RST7

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2619

Informations de copyright

Copyright © 2019 Csorba, Schirmbeck, Tuncer, Ribi, Roux-Lombard, Chizzolini, Huynh-Do, Vanhecke and Trendelenburg.

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Auteurs

Kinga Csorba (K)

Clinical Immunology, Department of Biomedicine and Division of Internal Medicine, University and University Hospital Basel, Basel, Switzerland.

Lucia A Schirmbeck (LA)

Clinical Immunology, Department of Biomedicine and Division of Internal Medicine, University and University Hospital Basel, Basel, Switzerland.

Eylul Tuncer (E)

Clinical Immunology, Department of Biomedicine and Division of Internal Medicine, University and University Hospital Basel, Basel, Switzerland.

Camillo Ribi (C)

Immunology and Allergy, Department of Internal Medicine, University Hospital Lausanne, Lausanne, Switzerland.

Pascale Roux-Lombard (P)

Division of Immunology and Allergy, Department of Medicine, University Hospital and University of Geneva, Geneva, Switzerland.

Carlo Chizzolini (C)

Division of Immunology and Allergy, Department of Medicine, University Hospital and University of Geneva, Geneva, Switzerland.

Uyen Huynh-Do (U)

Division of Nephrology and Hypertension, University Hospital Bern, Bern, Switzerland.

Dominique Vanhecke (D)

Clinical Immunology, Department of Biomedicine and Division of Internal Medicine, University and University Hospital Basel, Basel, Switzerland.

Marten Trendelenburg (M)

Clinical Immunology, Department of Biomedicine and Division of Internal Medicine, University and University Hospital Basel, Basel, Switzerland.

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