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Single-cell profiling reveals clonal CD8+T cell-derived IFNγ drives Sjögren's disease-related dacryoadenitis
Hao-Xian Zhu1,2, Fang-Fang Li1,2, Xiao-Min Chen1,3
1Chronic Disease Laboratory, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Summary
Clonally expanded CD8+ T cells producing IFNγ drive Sjögren's disease dacryoadenitis. Blocking IFNγ may offer a therapeutic strategy for this autoimmune condition.
Area of Science:
- Immunology
- Autoimmune Diseases
- Ophthalmology
Background:
- Sjögren's disease (SjD) is a chronic autoimmune disorder affecting exocrine glands.
- Dacryoadenitis is a common manifestation of SjD, but its mechanisms are unclear.
- Investigating the lacrimal gland's immune microenvironment is crucial for understanding SjD pathogenesis.
Purpose of the Study:
- To identify pathogenic immune cells and molecular factors in Sjögren's disease-related dacryoadenitis.
- To elucidate the role of the immune microenvironment in lacrimal gland dysfunction.
- To explore potential therapeutic targets for SjD-related dacryoadenitis.
Main Methods:
- Utilized Aire-/- mice as a model for Sjögren's disease-related dacryoadenitis.
- Employed single-cell RNA sequencing and flow cytometry to profile lacrimal gland immune cells.
- Investigated the role of IFNγ using Ifng-/-Aire-/- mice and assessed histopathological changes.
Main Results:
- Identified clonally expanded CCL5+CD8+ memory T cells expressing cytotoxic molecules near lacrimal acinar cells.
- Demonstrated that IFNγ from these T cells upregulates costimulatory molecules and chemokines.
- Observed significant reduction in inflammation and atrophy upon CD8+ T cell deletion or IFNγ knockout in Aire-/- mice.
Conclusions:
- IFNγ from clonally expanded CCL5+CD8+ memory T cells is a key driver of Sjögren's disease dacryoadenitis.
- These findings support IFNγ blockade as a potential therapeutic approach for SjD-related dacryoadenitis.
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