Inflammasomes in Sjögren's Disease: Exploring the Therapeutic Value
Margherita Sisto1, Sabrina Lisi1
1Department of Translational Biomedicine and Neuroscience (DiBraiN), Section of Human Anatomy and Histology, University of Bari "Aldo Moro", 70124 Bari, Italy.
International Journal of Molecular Sciences
|July 28, 2026
Summary
Aberrant inflammasome activation, particularly NLRP3 and AIM2, contributes to Sjögren
Area of Science:
- Immunology
- Molecular Biology
- Autoimmune Diseases
Background:
- Inflammasomes are crucial protein complexes regulating inflammation and innate immunity.
- Pathogen molecules or cellular damage trigger inflammasome assembly and activation.
- Dysregulated inflammasome activity is implicated in various autoimmune conditions.
Purpose of the Study:
- To review inflammasome assembly mechanisms.
- To elucidate the role of NLRP3 and AIM2 inflammasomes in Sjögren's disease (SjD).
Main Methods:
- Literature review focusing on inflammasome assembly and function.
- Analysis of studies linking NLRP3 and AIM2 inflammasomes to SjD pathogenesis.
Main Results:
- NLRP3 and AIM2 inflammasomes are implicated in SjD pathogenesis.
- Their aberrant activation drives chronic inflammation, leading to characteristic SjD symptoms.
- These inflammasomes are linked to an increased risk of B-cell non-Hodgkin's lymphoma in SjD patients.
Conclusions:
- Understanding NLRP3 and AIM2 inflammasome roles is key to SjD pathogenesis.
- Targeting these inflammasomes may offer novel therapeutic strategies for SjD.
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