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Type-I Interferons Inhibit Interleukin-10 Signaling and Favor Type 1 Diabetes Development in Nonobese Diabetic Mice
Marcos Iglesias1, Anirudh Arun1, Maria Chicco1
1Vascularized and Composite Allotransplantation Laboratory, Department of Plastic and Reconstructive Surgery, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Frontiers in Immunology
|August 1, 2018
Summary
Type-I interferons (TI-IFN) selectively block interleukin-10 (IL-10) signaling in T cells, impacting type 1 diabetes development. Restoring IL-10 signaling via TI-IFN blockade delays disease onset and reduces severity.
Area of Science:
- Immunology
- Endocrinology
- Molecular Biology
Background:
- Type 1 diabetes results from autoimmune destruction of insulin-producing beta-cells by T lymphocytes.
- Type-I interferons (TI-IFN) and interleukin-10 (IL-10) are implicated in type 1 diabetes, but their interaction in modulating T cells is unclear.
Purpose of the Study:
- To investigate the interplay between TI-IFN and IL-10 signaling in T cells during type 1 diabetes development.
- To explore the therapeutic potential of modulating this interaction.
Main Methods:
- Utilized nonobese diabetic mouse models.
- Analyzed T cell responses and IL-10 signaling pathways.
- Investigated the effects of TI-IFN blockade on disease progression.
Main Results:
- TI-IFN selectively inhibit IL-10 signaling in effector and regulatory T cells, affecting their function.
- This inhibition is localized to T cells in pancreatic and mesenteric lymph nodes in diabetic mice.
- Blocking TI-IFN/IFN-R interaction reversed IL-10 signaling inhibition, delayed diabetes onset, and reduced disease severity.
Conclusions:
- A novel molecular link between TI-IFN and IL-10 signaling in autoimmune diabetes is identified.
- This finding enhances understanding of autoimmune diabetes pathogenesis.
- Targeting the TI-IFN/IL-10 axis presents a potential therapeutic strategy for type 1 diabetes.
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