Abstract
NOD mice can be protected from transferred diabetes for long periods by short-term treatment with CD8 mabs. This protection has previously been shown to be thymus-dependent as thymectomised mice do not show the long-term protection observed in intact mice. In this study we show that the thymus is required only during antibody treatment as its removal thereafter does not affect protection. Recent thymic emigrants (RTEs) are not necessary for long-term tolerance induction and irradiation plays no part as anti-CD8 treatment cannot protect NOD.scid recipients from diabetes development. IL-10 is also shown to play an important role in the anti-CD8 induced protection in intact mice as it is reversed by IL-10R blockade.
Acknowledgements
The authors wish to express their gratitude to Professor Herman Waldmann and Dr Fiona Powrie for provision of hybridomas. We are indebted to Dr Jenny Phillips for production and provision of monoclonal antibodies. We are grateful to the Wellcome Trust for their support.