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Depletion of IL‐2 receptor β‐positive cells protects from diabetes in non‐obese diabetic mice
Author(s) -
Brauner Hanna,
Hall Håkan T,
FlodströmTullberg Malin,
Kärre Klas,
Höglund Petter,
Johansson Sofia
Publication year - 2016
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.2015.78
Subject(s) - diabetes mellitus , medicine , endocrinology , receptor , obesity
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.