irst of all we would like to thank Dr. von Herrath, who has long-standing experience in transgenic models in which autoimmunity is triggered by viral agents, and who has also been a close collaborator, for the very stimulating comments on our editorial article. It was indeed the aim of our opinion paper to generate debate. We are pleased that the editor has given us the opportunity to express our views in this reply. Concerning the mouse models, our purpose was to highlight the preclinical

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... tance of the spontaneous overtly diabetic, but not prediabetic, NOD female model. We agree that this is not, for obvious reasons, an easy model to handle and that some time is needed to get the best results from it. This does not mean at all, however, that CD3 antibodies did not show a high efficacy in other experimental models. We fully acknowledge K. Herold's work in the streptozotocininduced diabetes model in normal mice [1]. We ourselves provided evidence in support of the efficacy of CD3 antibody treatment in the cyclophosphamideinduced diabetes model in NOD mice [2, 3] and, in collaboration with Dr. von Herrath, the LCMVinduced diabetes model in LCMV GP-RIP transgenic mice [4] . The problem is, however, that in addition to CD3 antibodies, an exceedingly high number of other strategies were effective in disease prevention and/or treatment in these other models that were not active at Response to Comment by Bresson and von Herrath The Review of Diabetic Studies 191 Vol. 2 ⋅ No. 4 ⋅ 2005 www.The-RDS.org Rev Diabetic Stud (2005) 2:190-191