ArticleFrontiers in immunology2019
Anti-C1q Antibodies as Occurring in Systemic Lupus Erythematosus Could Be Induced by an Epstein-Barr Virus-Derived Antigenic Site.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.
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Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 44 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- Serological Evidence for the Association Between Epstein-Barr Virus Infection and Sjögren's Syndrome.Frontiers in immunology · 2020Pooled it
- Mechanisms of Epstein-Barr virus-associated autoimmunity: a comparative overview.Frontiers in immunology · 2026Review
- How Epstein Barr virus shapes lupus autoimmunity: mechanistic insights and therapeutic perspectives.Frontiers in immunology · 2026Review
- Epstein Barr virus antigen-induced autoantibodies against complement C1q exacerbate renal disease in lupus-prone mice.Frontiers in immunology · 2026Article
- Identification and Validation of ISG20 as a Shared Immune-Related Crosstalk Marker in Rheumatoid Arthritis and Inflammatory Bowel Disease.Journal of inflammation research · 2026Article
- Advancements in nanomedicine for the therapeutic regulation of efferocytosis: opportunities and challenges.Theranostics · 2026Review
- Detection rate, demographic associations and clinical implications of anti-C1q antibody elevations across diverse disease states.Lupus science & medicine · 2025Article
- Anti-C1q Autoantibody-Binding Engineered scFv C1q-Mimicking Fragment Enhances Disease Progression in Lupus-Prone MRL/lpr Mice.International journal of molecular sciences · 2025Article
- T and B cell responses against Epstein-Barr virus in primary sclerosing cholangitis.Nature medicine · 2025Article
- Decoding the etiology of immune-mediated inflammatory diseases statistically.Frontiers in immunology · 2025Review
- Epstein-Barr virus as a potentiator of autoimmune diseases.Nature reviews. Rheumatology · 2024Review
- Exploring the relationship between infectious agents and autoimmune diseases: a review.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2024Review
- Review
- Anti-C1q autoantibodies from systemic lupus erythematosus patients enhance CD40-CD154-mediated inflammation in peripheral blood mononuclear cellsClinical & translational immunology · 2022Article
- Complement C1s as a diagnostic marker and therapeutic target: Progress and propective.Frontiers in immunology · 2022Review
- A High Prevalence of Anti-EBNA1 Heteroantibodies in Systemic Lupus Erythematosus (SLE) Supports Anti-EBNA1 as an Origin for SLE Autoantibodies.Frontiers in immunology · 2022Article
- Anti-Idiotype scFv Localizes an Autoepitope in the Globular Domain of C1q.International journal of molecular sciences · 2021Article
- Review
- Autoantibodies against complement component C1q in systemic lupus erythematosus.Clinical & translational immunology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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
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