Annals of the rheumatic diseases · 2024
Evidence that autoantibody production may be driven by acute Epstein-Barr virus infection in Sjögren's disease.
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Hudson Erin, Yang Lijun, Chu Elizabeth K, Zhuang Haoyang, Arja Rawad Daniel, Betancourt Blas Y, Bhattacharyya Indraneel, Han Shuhong, Cha Seunghee, Chan Edward K L, Sebastian Mathew, Stalvey Carolyn, Fritzler Marvin J, Reeves Westley H
Аннотация
OBJECTIVES: Sjögren's disease (SD) is an autoimmune disease affecting the exocrine glands that is associated with autoantibodies against Ro60/SS-A, anti-Ro52/TRIM21, La/SS-B and others. We examined the role of acute Epstein-Barr virus (EBV) infection in the pathogenesis of these autoantibodies in a previously healthy patient (patient 1) with primary EBV infection who developed SD with anti-Ro/La and anti-Smith/U1 ribonucleoprotein (Sm/U1RNP) autoantibodies and had lymphoplasmacytic foci on labial salivary gland biopsy.
METHODS: Immune responses to Epstein-Barr nuclear antigen-1 (EBNA1) and the Ro52/Ro60/La and Sm/U1RNP autoantigens and peptides were examined by immunoassay in patient 1, healthy and disease controls.
RESULTS: Anti-Ro52 and anti-Ro60 autoantibodies were present 7 days after primary infection and underwent IgM to IgG switching, suggesting that EBV infection promoted their production. More than 7 months after primary infection, new and increasing levels of antibodies against EBNA1 and the U1RNP autoantigen appeared concomitantly. These antibodies bound homologous peptide sequences shared by EBNA1, SmB' and the U1-C (U1RNP) protein, consistent with induction by molecular mimicry. Although Ro60 and EBNA1 crossreact immunologically, we found that anti-Ro60/anti-Ro52 antibody production was stimulated by acute EBV infection long before the onset of anti-EBNA1. Unexpectedly, a subset of healthy control sera had anti-SmB' peptide antibodies that were not correlated with anti-EBNA1 peptide antibodies. In contrast, anti-SmB' and EBNA1 peptide antibody levels correlated in anti-Sm/U1RNP+ lupus sera.
CONCLUSIONS: Primary EBV infection can promote anti-Ro60/anti-Ro52 and anti-U1RNP responses, though by different mechanisms. Some healthy individuals produce anti-SmB' peptide autoantibodies independently of a response to EBNA1.
METHODS: Immune responses to Epstein-Barr nuclear antigen-1 (EBNA1) and the Ro52/Ro60/La and Sm/U1RNP autoantigens and peptides were examined by immunoassay in patient 1, healthy and disease controls.
RESULTS: Anti-Ro52 and anti-Ro60 autoantibodies were present 7 days after primary infection and underwent IgM to IgG switching, suggesting that EBV infection promoted their production. More than 7 months after primary infection, new and increasing levels of antibodies against EBNA1 and the U1RNP autoantigen appeared concomitantly. These antibodies bound homologous peptide sequences shared by EBNA1, SmB' and the U1-C (U1RNP) protein, consistent with induction by molecular mimicry. Although Ro60 and EBNA1 crossreact immunologically, we found that anti-Ro60/anti-Ro52 antibody production was stimulated by acute EBV infection long before the onset of anti-EBNA1. Unexpectedly, a subset of healthy control sera had anti-SmB' peptide antibodies that were not correlated with anti-EBNA1 peptide antibodies. In contrast, anti-SmB' and EBNA1 peptide antibody levels correlated in anti-Sm/U1RNP+ lupus sera.
CONCLUSIONS: Primary EBV infection can promote anti-Ro60/anti-Ro52 and anti-U1RNP responses, though by different mechanisms. Some healthy individuals produce anti-SmB' peptide autoantibodies independently of a response to EBNA1.