ArticleBiochimica et biophysica acta. Molecular basis of disease2018
Anti-IL-7 receptor-α treatment ameliorates newly established Sjögren's-like exocrinopathy in non-obese diabetic mice.
Article in Biochimica et biophysica acta. Molecular basis of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Composition and regulation of the immune microenvironment of salivary gland in Sjögren's syndrome.Frontiers in immunology · 2022Pooled it
- SARS-CoV-2 spike protein induces salivary gland dysfunction and immune infiltration in C57BL/6 mice.Frontiers in immunology · 2025Article
- Altered characteristics of regulatory T cells in target tissues of Sjögren's syndrome in murine models.Molecular immunology · 2024Article
- The impact of alternate-day fasting on the salivary gland stem cell compartments in non-obese diabetic mice with newly established Sjögren's syndrome.Biochimica et biophysica acta. Molecular cell research · 2024Article
- Endogenous IL-22 contributes to the pathogenesis of salivary gland dysfunction in the non-obese diabetic model of Sjögren's syndrome.Molecular immunology · 2024Article
- Immune and non-immune mediators in the fibrosis pathogenesis of salivary gland in Sjögren's syndrome.Frontiers in immunology · 2024Review
- The involvement of aquaporin 5 in the inflammatory response of primary Sjogren's syndrome dry eye: potential therapeutic targets exploration.Frontiers in medicine · 2024Review
- Subpopulation dynamics of T and B lymphocytes in Sjögren's syndrome: implications for disease activity and treatment.Frontiers in immunology · 2024Review
- Inhibition of NLRP3 inflammasome activity by MCC950 leads to exacerbation of Sjӧgren's syndrome pathologies in non-obese diabetic mice.Immunology · 2023Article
- Alternate-Day Fasting Ameliorates Newly Established Sjögren's Syndrome-like Sialadenitis in Non-Obese Diabetic Mice.International journal of molecular sciences · 2022Article
- Molecular Mechanisms Linking Inflammation to Autoimmunity in Sjögren's Syndrome: Identification of New Targets.International journal of molecular sciences · 2022Review
- Interleukin-22 Exerts Detrimental Effects on Salivary Gland Integrity and Function.International journal of molecular sciences · 2022Article
- JAK/STAT Pathway Targeting in Primary Sjögren Syndrome.Rheumatology and immunology research · 2022Review
- Plasmacytoid dendritic cells promote the pathogenesis of Sjögren's syndrome.Biochimica et biophysica acta. Molecular basis of disease · 2022Article
- Low Dose Interleukin-2 Ameliorates Sjögren's Syndrome in a Murine Model.Frontiers in medicine · 2022Article
- Biologic therapy in Sjögren's syndrome.Clinical rheumatology · 2021Review
- T Cells Subsets in the Immunopathology and Treatment of Sjogren's Syndrome.Biomolecules · 2020Review
- Insight into Salivary Gland Aquaporins.Cells · 2020Review
- Involvement of Aquaporins in the Pathogenesis, Diagnosis and Treatment of Sjögren's Syndrome.International journal of molecular sciences · 2018Review
- Type I Interferon Signaling Is Required for Dacryoadenitis in the Nonobese Diabetic Mouse Model of Sjögren Syndrome.International journal of molecular sciences · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The levels of interleukin (IL)-7 and its receptor are elevated in the salivary glands of patients with Sjögren's syndrome (SS). Our previous study indicates that IL-7 plays a critical pathogenic role in the development and onset of SS in a mouse model of this disease. The present study aims at determining whether IL-7 also plays a role in sustaining SS pathologies after the disease onset, by using the non-obese diabetic (NOD) model. Intraperitoneal administration of a blocking antibody against the IL-7 receptor α chain (IL-7Rα) to female NOD mice aged 10 weeks, which exhibited newly onset clinical SS, for the duration of 3 weeks significantly ameliorated characteristic SS pathologies including hyposalivation and leukocyte infiltration of the submandibular glands (SMGs). These changes were accompanied by a decrease in IFN-γ-producing CD4 T- and CD8 T cells, B cells, and lymphocyte chemoattractants CXCL9, -10, -11 and -13 in the SMGs. Anti-IL-7Rα treatment markedly diminished the amount of TNF-α in the SMGs and increased the level of claudin-1 and aquaporin 5, two molecules critical for normal salivary secretion. Furthermore, neutralization of IFN-γ and TNF-α, individually or in combination, considerably improved salivary secretion, reduced leukocyte infiltration and down-regulated CXCL9 and -13 expression in the SMGs. Collectively, the results indicate that endogenous IL-7R signals promote Th1 and Tc1 responses and IFN-γ- and TNF-α production to sustain the persistence of SS-like sialadenitis in NOD mice. These findings suggest that IL-7 and Th1 cytokines could serve as promising therapeutic targets for this prevalent autoimmune disease.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.