ArticleImmunology and cell biology2016
Depletion of IL-2 receptor β-positive cells protects from diabetes in non-obese diabetic mice.
Article in Immunology and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- IL-15Rα-Independent IL-15 Signaling in Non-NK Cell-Derived IFNγ Driven Control ofFrontiers in immunology · 2021Article
- Decoding inflammation, its causes, genomic responses, and emerging countermeasures.Scandinavian journal of immunology · 2019Review
- Advances in the Study of CD8+ Regulatory T Cells.Critical reviews in immunology · 2019Review
- CD122 blockade restores immunological tolerance in autoimmune type 1 diabetes via multiple mechanisms.JCI insight · 2018Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The destruction of β-cells in type 1 diabetes (T1D) progresses silently until only a minor fraction of the β-cells remain. A late acting therapy leading to the prevention of further β-cell killing would therefore be desirable. CD122, the β chain of the interleukin-2 receptor, is highly expressed on natural killer (NK) cells and on a subpopulation of CD8 T cells. In this study, we have treated non-obese diabetic (NOD) mice with a depleting antibody against CD122. The treatment protected from diabetes, even when initiated just before disease onset. The degree of leukocyte infiltration into islets was unaffected by the treatment, further supporting effectiveness late in the disease process. It effectively removed all NK cells from the spleen, pancreas and pancreatic lymph nodes and abolished NK cell activity. Interestingly, despite the lack of CD122 expression on CD8 T cells in the pancreas, the overall frequency of CD8 cells decreased in this organ, whereas it was unaffected in the spleen. T cells were also still capable to respond against a foreign antigen. Conclusively, targeting of CD122(+) cells could represent a novel treatment strategy against T1D.
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