ArticleJournal of immunology (Baltimore, Md. : 1950)2017
SATB1 Conditional Knockout Results in Sjögren's Syndrome in Mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Advances in Pathogenesis of Sjögren's Syndrome.Journal of immunology research · 2021Pooled it
- Aging-associated SATB1 deficiency remodels 3D genome architecture and transcriptional programs in naive CD4Science advances · 2026Article
- mTOR signaling pathway in primary Sjögren's syndrome: Pathogenesis and potential therapeutic targets (Review).International journal of molecular medicine · 2026Review
- Establishment of Autoreactive CD4International journal of molecular sciences · 2025Article
- Article
- Sjögren's Syndrome: Epidemiology, Classification Criteria, Molecular Pathogenesis, Diagnosis, and Treatment.MedComm · 2025Review
- Common pathological mechanisms and therapeutic strategies in primary Sjogren's syndrome and primary biliary cholangitis: from tissue immune microenvironment to targeted therapy.Frontiers in immunology · 2025Review
- SATB1 prevents immune cell infiltration by regulating chromatin organization and gene expression of a chemokine gene cluster in T cells.Communications biology · 2024Article
- Vasoactive intestinal peptide exerts therapeutic action by regulating PTEN in a model of Sjögren's disease.Immunity, inflammation and disease · 2023Article
- SATB1 ensures appropriate transcriptional programs within naïve CD8Immunology and cell biology · 2022Article
- 3D Genome Organization as an Epigenetic Determinant of Transcription Regulation in T Cells.Frontiers in immunology · 2022Review
- SATB1-dependent mitochondrial ROS production controls TCR signaling in CD4 T cells.Life science alliance · 2021Article
- Increased Indoleamine 2,3-Dioxygenase Levels at the Onset of Sjögren's Syndrome in SATB1-Conditional Knockout Mice.International journal of molecular sciences · 2021Article
- Review
- Salivary-gland-protective regulatory T-cell dysfunction underlies female-specific sialadenitis in the non-obese diabetic mouse model of Sjögren syndrome.Immunology · 2018Article
- A Role for Satb1 in Thyroid Autoimmunity?Thyroid : official journal of the American Thyroid Association · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sjögren's syndrome (SS) is an autoimmune disease in which exocrine tissues are affected by cellular and humoral immunity. As a result, the salivary and lacrimal glands of patients with SS are damaged, leading to xerostomia (dry mouth) and keratoconjunctivitis sicca (dry eyes). Because experimental approaches to investigate SS pathogenesis in human patients are limited, development of a mouse model is indispensable for understanding the disease. In this study, we show that special AT-rich sequence binding protein-1 conditional knockout (SATB1cKO) mice, in which the SATB1 gene is specifically deleted from hematopoietic cells, develop SS by 4 wk of age, soon after weaning. Female mice presented an earlier onset of the disease than males, suggesting that female SATB1cKO mice are more susceptible to SS. T cell-dominant immune cell infiltration was observed in the salivary glands of 4 wk old SATB1cKO mice, and the frequency of B cells gradually increased as the mice aged. Consistently, levels of anti-SSA and anti-SSB Abs were increased around 8 wk of age, after salivary production reached its lowest level in SATB1cKO mice. These results suggest that SATB1cKO mice can be a novel SS model, in which the progression and characteristics of the disease resemble those of human SS.
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Registered trials
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