Epstein-Barr Virus-Induced Upregulation of GPR183: A Potential Upstream Mechanism in IgG4-Related Ophthalmic…

StudyInvestigative ophthalmology & visual science· Jul 2026

Epstein-Barr Virus-Induced Upregulation of GPR183: A Potential Upstream Mechanism in IgG4-Related Ophthalmic Disease.

Zhengze Sun, Jichao Zhou, Yi Wang … Hong Qi

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OculoplasticsStudyQ1IF 4.2

Epstein-Barr virus infection is strongly linked to IgG4-related eye disease

Epstein-Barr Virus-Induced Upregulation of GPR183: A Potential Upstream Mechanism in IgG4-Related Ophthalmic Disease.

Zhengze Sun … Hong Qi

Investigative ophthalmology & visual science · Jul 2026 · Q1 in Ophthalmology

Background

Immunoglobulin G4-related ophthalmic disease (IgG4-ROD) is the most common subtype of IgG4-related disease (IgG4-RD), yet its pathogenic mechanisms remain poorly understood.

Purpose

This study aimed to identify potential upstream triggers of IgG4-ROD and novel therapeutic targets.

Methods

Fourteen patients with IgG4-ROD and 13 controls (9 with lacrimal gland prolapse and 4 with chronic dacryoadenitis) were enrolled.

n = 13 controls

Results

most IgG4-ROD eye tissue samples tested positive for Epstein-Barr virus, far more than controls

IgG4-ROD

85.7%

Controls

15.4%

More results

GPR183 was broadly expressed across multiple immune cell populations in lacrimal glands.

Multiplex immunofluorescence demonstrated prominent GPR183 expression within ectopic germinal centers, particularly in B-lymphocyte-rich regions.

Epstein-Barr virus DNA copy number positively correlated with serum IgG4 levels (adjusted R² = 0.79, P < 0.01).

More results

Epstein-Barr virus markers EBNA1 and LMP1 were co-expressed with GPR183.

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Conclusion

Our findings suggest that Epstein-Barr virus-induced GPR183 upregulation potentially promotes ectopic germinal center formation and contributes to the pathogenesis of IgG4-ROD.

Epstein-Barr Virus-Induced Upregulation of GPR183: A Potential Upstream Mechanism in IgG4-Related Ophthalmic Disease.

Epstein-Barr Virus-Induced Upregulation of GPR183: A Potential Upstream Mechanism in IgG4-Related Ophthalmic Disease.

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