**2. Introduction**

Even though patients with T1D need insulin, the primary goal of novel therapies is to preserve residual insulin secretion, in best case to cure diabetes or at least to make the disease milder

© 2013 Ludvigsson; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

and facilitate treatment. Patients with residual insulin secretion usually get lower HbA1c, and residual insulin secretion facilitates the treatment, decreases the risk for serious hypoglycaemia and the risk of keto-acidosis [10]. Already very modest beta cell function, with peak stimulated C-peptide above 0.2 nmol/L seems to reduce long-term complications [11]. Furthermore, Cpeptide per se has been proposed to decrease the risk of complications, especially neuropathy. There is increasing evidence that C-peptide is not just a connecting peptide to keep the two insulin chains in in a certain structure, but a hormone with several important effects [12]. The relevance of saving beta cells and improving their function has become even more evident when studies suggest that beta cells may regenerate [13, 14]. If this is the case an end of the destructive process might lead to cure of T1D [15].

interventions in healthy children with increased risk of developing T1D except for children

Immune Intervention in Type I Diabetes Mellitus

http://dx.doi.org/10.5772/52801

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**Figure 1.** At a Nordic symposium in connection with Annual meeting of Scandinavian Society for the Study of Diabe‐ tes, Linköping 1981, the author showed this slide. Type 1diabetes was proposed to develop after a long autoimmune process destroying the beta cells. Events during pregnancy and the importance of breast-feeding was suggested, and

After encouraging Phase II trials two different Phase III trials using antiCD3 failed to reach their primary endpoints [33,34], but one of them, the Protégé study, did show efficacy in younger patients age 8-18 years when a reasonably high dose of antiCD-3 was used [34]. This was especially true in certain patient populations (mainly patients in USA, but also in Europe) who had rather well preserved C-peptide, often near-normal HbA1c and low insulin require‐ ment. Further studies are needed to learn what doses are efficient without severe adverse events, and in what patient populations the treatment works best. The old policy defended by many diabetologists to treat all so called T1D in the same way irrespective of age, ethnic back‐

Traditional vaccinations could either contribute to the development of T1D, or T1D could be prevented by vaccination. Already in the 1920ies mumps infection was shown to be a possible

later shown to be relevant, and regeneration of beta cells was proposed as a possibility.

ground, severity of disease at diagnosis etc may probably have to be left.

**5. Vaccines against infections**

with extremely high risk of developing T1D close in time.
