NLRP3 inflammasome and Sjögren disease: mechanisms, clinical associations and therapeutic prospects
4 affiliations
- 1Heilongjiang University of Chinese Medicine
- 2Heilongjiang Provincial Hospital
- 3The Second Hospital of Heilongjiang Province
- 4The First Affiliated Hospital of Heilongjiang University of Chinese Medicine
Abstract
Sjögren disease (SjD; formerly referred to as Sjögren syndrome) is a chronic autoimmune disease characterized by exocrine gland dysfunction and systemic immune abnormalities. In recent years, clinical and preclinical studies have suggested that dysregulation of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome may contribute to inflammatory responses, glandular damage, and disease progression in SjD, although the available human evidence remains primarily associative. This review summarizes alterations in the NLRP3 inflammasome in patients with SjD, animal models, and cell models; discusses its upstream regulation, downstream effects, associated clinical phenotypes, and systemic involvement; and compares evidence across different cell types, disease stages, and therapeutic interventions. Based on current evidence, NLRP3 is more likely to function as an inflammatory amplification and regulatory node in the context of pre-existing autoimmunity and tissue stress, with its role varying according to cell type, disease status, and the local microenvironment. NLRP3 and its related pathways therefore have potential therapeutic value; however, evidence for direct targeting of NLRP3 in SjD remains largely limited to preclinical studies, whereas some immunomodulatory drugs supported by clinical studies are not NLRP3-specific therapies. Further clarification of the cell-specific and stage-specific roles of NLRP3, together with identification of patient subgroups that may benefit, will be critical for promoting its clinical translation.
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BibTeX
@article{niu2026nlrp3,
title = {{NLRP3 inflammasome and Sjögren disease: mechanisms, clinical associations and therapeutic prospects}},
author = {Rui Niu and Qiwei Li and Linwei Li and Qingai Guo and Jiayi Zhao and Xiadong Yang and Shouze Ren and Lina Zhao and Chang Liu and Ying Ma and Peng Zhou and Jingyuan Li and Zeguang Li and Hua Liang},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.2004934},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.2004934/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - NLRP3 inflammasome and Sjögren disease: mechanisms, clinical associations and therapeutic prospects
AU - Rui Niu
AU - Qiwei Li
AU - Linwei Li
AU - Qingai Guo
AU - Jiayi Zhao
AU - Xiadong Yang
AU - Shouze Ren
AU - Lina Zhao
AU - Chang Liu
AU - Ying Ma
AU - Peng Zhou
AU - Jingyuan Li
AU - Zeguang Li
AU - Hua Liang
PY - 2026
DA - 2026/10/30
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.2004934
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.2004934/full
AB - Sjögren disease (SjD; formerly referred to as Sjögren syndrome) is a chronic autoimmune disease characterized by exocrine gland dysfunction and systemic immune abnormalities. In recent years, clinical and preclinical studies have suggested that dysregulation of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome may contribute to inflammatory responses, glandular damage, and disease progression in SjD, although the available human evidence remains primarily associative. This review summarizes alterations in the NLRP3 inflammasome in patients with SjD, animal models, and cell models; discusses its upstream regulation, downstream effects, associated clinical phenotypes, and systemic involvement; and compares evidence across different cell types, disease stages, and therapeutic interventions. Based on current evidence, NLRP3 is more likely to function as an inflammatory amplification and regulatory node in the context of pre-existing autoimmunity and tissue stress, with its role varying according to cell type, disease status, and the local microenvironment. NLRP3 and its related pathways therefore have potential therapeutic value; however, evidence for direct targeting of NLRP3 in SjD remains largely limited to preclinical studies, whereas some immunomodulatory drugs supported by clinical studies are not NLRP3-specific therapies. Further clarification of the cell-specific and stage-specific roles of NLRP3, together with identification of patient subgroups that may benefit, will be critical for promoting its clinical translation.
SN - 1664-3224
ER -