ArticleImmunology2018
Salivary-gland-protective regulatory T-cell dysfunction underlies female-specific sialadenitis in the non-obese diabetic mouse model of Sjögren syndrome.
Article in Immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- Hormonal risk factors and androgen and glucocorticoid dysregulation in Sjogren's disease and non-Sjogren's sicca.Rheumatology (Oxford, England) · 2026Article
- Altered characteristics of regulatory T cells in target tissues of Sjögren's syndrome in murine models.Molecular immunology · 2024Article
- Investigative biological therapies for primary Sjögren's syndrome.Archives of medical science : AMS · 2024Article
- Added value of lymphocyte subpopulations in the classification of Sjögren's syndrome.Scientific reports · 2023Article
- A combination treatment of low-dose dexamethasone and aspirin-triggered resolvin D1 reduces Sjögren syndrome-like features in a mouse model.JADA foundational science · 2023Article
- Advances in regenerative medicine applications of tetrahedral framework nucleic acid-based nanomaterials: an expert consensus recommendation.International journal of oral science · 2022Review
- MSC-Derived Small Extracellular Vesicles Attenuate Autoimmune Dacryoadenitis by Promoting M2 Macrophage Polarization and Inducing TregsFrontiers in immunology · 2022Article
- Quantitative Scintigraphy Evaluated the Relationship between 131I Therapy and Salivary Glands Function in DTC Patients: A Retrospective Analysis.Journal of healthcare engineering · 2022Article
- Characterization of Type I Interferon-Associated Chemokines and Cytokines in Lacrimal Glands of Nonobese Diabetic Mice.International journal of molecular sciences · 2021Article
- Toll-Like Receptor 7 Is Required for Lacrimal Gland Autoimmunity and Type 1 Diabetes Development in Male Nonobese Diabetic Mice.International journal of molecular sciences · 2020Article
- Mesenchymal stem cells inhibited the differentiation of MDSCs via COX2/PGE2 in experimental sialadenitis.Stem cell research & therapy · 2020Article
- UBASH3A deficiency accelerates type 1 diabetes development and enhances salivary gland inflammation in NOD mice.Scientific reports · 2020Article
- Sex-mediated elevation of the specialized pro-resolving lipid mediator levels in a Sjögren's syndrome mouse model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- The gut-eye-lacrimal gland-microbiome axis in Sjögren Syndrome.The ocular surface · 2020Review
- Carnitine Palmitoyl Transferase Deficiency in a University Immunology Practice.Current rheumatology reports · 2020Review
- Hyperglycemia and Salivary Gland Dysfunction in the Non-obese Diabetic Mouse: Caveats for Preclinical Studies in Sjögren's Syndrome.Scientific reports · 2019Article
- Type I Interferon Signaling Is Required for Dacryoadenitis in the Nonobese Diabetic Mouse Model of Sjögren Syndrome.International journal of molecular sciences · 2018Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Immune cell-mediated destruction of salivary glands is a hallmark feature of Sjögren syndrome. Similar to the female predominance in humans, female non-obese diabetic (NOD) mice develop spontaneous salivary gland autoimmunity. However, in both humans and mice it is unclear what factors contribute to the initial immune infiltration of the salivary glands. Here, we used an adoptive transfer model of Sjögren syndrome to determine if female mice harbor a sex-specific defect in salivary-gland-protective regulatory T (Treg) cells. Transfer of cervical lymph node (LN) cells from female NOD mice into sex-matched NOD-severe combined immunodeficient (SCID) recipients resulted in sialadenitis, regardless of the presence or absence of Treg cells. In contrast, transfer of cervical LN cells from male NOD mice into sex-matched NOD-SCID recipients only resulted in sialadenitis when Treg cells were depleted before transfer, suggesting that male NOD mice have functional salivary-gland-protective Treg cells. Notably, the host environment affected the ability of Treg cells to prevent sialadenitis with testosterone promoting salivary gland protection. Treg cells from male mice did not protect against sialadenitis in female recipients. Testosterone treatment of female recipients of bulk cervical LN cells decreased sialadenitis, and Treg cells from female mice were capable of protecting against development of sialadenitis in male recipients. Hence, our data demonstrate that female NOD mice develop sialadenitis through a defect in salivary-gland-protective Treg cells that can be reversed in the presence of testosterone.
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