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Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
Published on: May 6, 2013
IL-17 immunity in human type 1 diabetes.
Jarno Honkanen1, Janne K Nieminen, Ru Gao
1Immune Response Unit, National Institute for Health and Welfare, Helsinki, Finland.
Journal of Immunology (Baltimore, Md. : 1950)
|July 2, 2010
Summary
T helper 17 (Th17) immunity is upregulated in children with type 1 diabetes (T1D). Interleukin-17 (IL-17) exacerbates islet cell damage, suggesting a role for Th17 immunity in T1D pathogenesis and potential therapeutic targets.
Area of Science:
- Immunology
- Endocrinology
- Autoimmunity
Background:
- Th17 immunity regulates autoimmune diabetes in mice, but its role in human type 1 diabetes (T1D) is unclear.
- IL-17 neutralization impacts disease progression in mice, suggesting involvement in the effector phase.
Purpose of the Study:
- To investigate the role and characteristics of Th17 immunity in human T1D.
- To determine the effects of IL-17 on human islet cells.
Main Methods:
- Analysis of T helper 17 (Th17) immunity in peripheral blood T cells from children with T1D.
- Measurement of IL-17, IL-22, FOXP3, and IFN-gamma expression in activated T cells and circulating memory CD4 cells.
- In vitro assessment of IL-17 effects on human islet cells.
Main Results:
- Upregulation of Th17 immunity, including increased IL-17 and IL-22 secretion and FOXP3 transcripts, observed in children with T1D.
- Evidence of in vivo IL-17 pathway activation in circulating memory CD4 cells.
- IL-17 demonstrated detrimental effects on human islet cells, potentiating inflammatory and proapoptotic responses.
Conclusions:
- Th17 immunity plays a significant role in the pathogenesis of human T1D.
- IL-17 pathway activation is implicated in T1D.
- Findings suggest IL-17 as a potential therapeutic target for T1D.
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