ArticleHistochemistry and cell biology2011
A failure of TNFAIP3 negative regulation maintains sustained NF-κB activation in Sjögren's syndrome.
Article in Histochemistry and cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 55 citations in OpenAlex.
- T Cell Transcriptomes from Paroxysmal Nocturnal Hemoglobinuria Patients Reveal Novel Signaling Pathways.Journal of immunology (Baltimore, Md. : 1950) · 2017Trial
- Tumor necrosis factor alpha-induced protein 3: A key biomarker for response to ursodeoxycholic acid in primary biliary cholangitis.World journal of hepatology · 2025Article
- Conjunctival MicroRNA Expression Signature in Primary Sjögren's Syndrome Dry Eye: A NanoString-Based Bioinformatic Analysis.Investigative ophthalmology & visual science · 2025Article
- TNFAIP3 alleviates pain in lumbar disc herniation rats by inhibiting the NF-κB pathway.Annals of translational medicine · 2022Article
- Protective effects of miR-155-5p silencing on IFN-γ-induced apoptosis and inflammation in salivary gland epithelial cells.Experimental and therapeutic medicine · 2021Article
- Epithelial-immune cell interplay in primary Sjögren syndrome salivary gland pathogenesis.Nature reviews. Rheumatology · 2021Review
- Pathogenetic Mechanisms Implicated in Sjögren's Syndrome Lymphomagenesis: A Review of the Literature.Journal of clinical medicine · 2020Review
- Understanding the Complexity of Sjögren's Syndrome: Remarkable Progress in Elucidating NF-κB Mechanisms.Journal of clinical medicine · 2020Review
- The PANoptosome: A Deadly Protein Complex Driving Pyroptosis, Apoptosis, and Necroptosis (PANoptosis).Frontiers in cellular and infection microbiology · 2020Review
- Expanding the spectrum of A20 haploinsufficiency in two Chinese families: cases report.BMC medical genetics · 2019Article
- Salivary Gland Stem Cells Age Prematurely in Primary Sjögren's Syndrome.Arthritis & rheumatology (Hoboken, N.J.) · 2019Article
- SNP variations in IL10, TNFα and TNFAIP3 genes in patients with dry eye syndrome and Sjogren's syndrome.Journal of inflammation (London, England) · 2019Article
- B cells in the pathogenesis of primary Sjögren syndrome.Nature reviews. Rheumatology · 2018Review
- TNFAIP3 F127C Coding Variation in Greek Primary Sjogren's Syndrome Patients.Journal of immunology research · 2018Article
- Update on Pathogenesis of Sjogren's Syndrome.Current rheumatology reviews · 2017Review
- Downstream activation of NF-κB in the EDA-A1/EDAR signalling in Sjögren's syndrome and its regulation by the ubiquitin-editing enzyme A20.Clinical and experimental immunology · 2016Article
- Roles of A20 in autoimmune diseases.Immunologic research · 2016Review
- Local and Systemic IKKε and NF-κB Signaling Associated with Sjögren's Syndrome Immunopathogenesis.Journal of immunology research · 2015Article
- Cystic Fibrosis from Laboratory to Bedside: The Role of A20 in NF-κB-Mediated Inflammation.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2015Review
- Rituximab-mediated Raf kinase inhibitor protein induction modulates NF-κB in Sjögren syndrome.Immunology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sjögren's syndrome (SS) is characterized by the features of systemic autoimmunity and exocrine gland dysfunction and inflammation. Deregulated cytokine production is known to contribute to the etiology of SS but the underlying molecular mechanism is still remains to be unclear. TNF-α-induced protein 3 or TNFAIP3 is involved in the negative feedback regulation of nuclear factor-κB (NF-κB) signaling in response to specific pro-inflammatory stimuli in different cell types. To define the contribution of TNFAIP3 to SS, the levels of TNFAIP3 expression in human salivary gland epithelial cells (SGEC) derived from active primary SS patients were analyzed. Histological analysis was performed on paraffin-embedded human Sjögren's samples and healthy tissues. In separate experiments, immunofluorescence staining, western blot analysis and quantitative real-time PCR for TNFAIP3 was conducted in SGEC from SS and healthy subjects. Our findings clearly demonstrate changes in levels of the protein and gene expression between healthy controls and SS patients, depicting a very weak positivity for TNFAIP3 in SS samples. TNFAIP3 was found down-regulated in SGECs derived from SS patients in comparison with controls, and the cells with down-regulated TNFAIP3 expression exhibited enhanced NF-κB activities. In addition, to investigate the role of TNFAIP3 in the activation of NF-κB, we depleted TNFAIP3 expression by siRNA in healthy SGEC after treatment with or without TNF-α. Intriguingly, the silencing of TNFAIP3 by its siRNA in healthy SGEC increased NF-κB activation that could explain the deregulated cytokines production observed in SS.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.