ArticleFrontiers in immunology2018
Type-I Interferons Inhibit Interleukin-10 Signaling and Favor Type 1 Diabetes Development in Nonobese Diabetic Mice.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Altered B cell metabolic pathways characterize type 1 diabetes progression.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- The Role of Type I Interferons in Tuberculosis and in Tuberculosis-Risk-Associated Comorbidities.Infectious disease reports · 2025Review
- Advancing Understanding of Epilepsy and Type 1 Diabetes Mellitus: A Global Perspective on Research Trends and Future Directions.Journal of diabetes research · 2025Article
- T cell responsiveness to IL-10 defines the immunomodulatory effect of costimulation blockade via anti-CD154 and impacts transplant survival.bioRxiv : the preprint server for biology · 2024Article
- The Relationship between Type 1 Diabetes Mellitus, TNF-α, and IL-10 Gene Expression.Biomedicines · 2023Article
- RNA Flow Cytometry for the Study of T Cell Metabolism.International journal of molecular sciences · 2021Review
- A cytokine super cyclone in COVID-19 patients with risk factors: the therapeutic potential of BCG immunization.Cytokine & growth factor reviews · 2020Review
- Innate Viral Sensor MDA5 and Coxsackievirus Interplay in Type 1 Diabetes Development.Microorganisms · 2020Review
- Cytokines in type 1 diabetes: mechanisms of action and immunotherapeutic targets.Clinical & translational immunology · 2020Review
- IL-33 Prevents MLD-STZ Induction of Diabetes and Attenuate Insulitis in Prediabetic NOD Mice.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Destruction of insulin-producing β-cells by autoreactive T lymphocytes leads to the development of type 1 diabetes. Type-I interferons (TI-IFN) and interleukin-10 (IL-10) have been connected with the pathophysiology of this disease; however, their interplay in the modulation of diabetogenic T cells remains unknown. We have discovered that TI-IFN cause a selective inhibition of IL-10 signaling in effector and regulatory T cells, altering their responses. This correlates with diabetes development in nonobese diabetic mice, where the inhibition is also spatially localized to T cells of pancreatic and mesenteric lymph nodes. IL-10 signaling inhibition is reversible and can be restored
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