Does partial preservation of residual beta-cell function justify immune intervention in recent onset Type I diabetes?

Immune intervention seems to offer the prospect of preventing or reversing the hyperglycaemic phase of Type I (insulin-dependent) diabetes mellitus. A number of prevention trials have been undertaken before disease onset but the logistics of such trials are prohibitive. More rapid and less expensive means of testing new therapies are needed and the current emphasis is therefore on intervention after diagnosis to salvage residual beta-cell function. At present, because restoration of normal metabolism seems unattainable, such interventions are tested against their ability to maintain C-peptide production over the first months or years of diabetes. C-peptide provides a useful surrogate measure of response with which to identify therapies that might justify more exhaustive investigation at an earlier stage of the disease process. As immune intervention is potentially harmful, the risks and benefits of participation in such trials require careful consideration. Therefore what is the evidence that preservation of residual insulin secretion provides clinical benefit to the patient? Trials capable of proving a direct causal link are lacking and might not be feasible. There is, however, a wealth of indirect evidence which requires careful scrutiny and debate, since this provides the basis for current attempts at immunotherapy.