Predicting Adult-Onset Autoimmune Diabetes

Clarity From Complexity

  1. R. David Leslie
  1. From the Blizard Institute of Cell and Molecular Science, London, U.K.
  1. Corresponding author: R. David Leslie, r.d.g.leslie{at}qmul.ac.uk.

“What is time?” asked Saint Augustine in his Confessions, “When someone asks me, I know. But as soon as someone comes to question me on this matter, and I try to explain, I don't know anymore.” A physician asked to define an autoimmune disease has a similar sense of frustration. For the perplexed, three features of autoimmune diseases, derived from Witebsky's postulates, might help: 1) the presence of defined autoantigens and autoantibodies; 2) passive transfer of T-lymphocytes, which leads to disease development; and 3) successful immunomodulation of disease (1). Indeed, for type 1 diabetes in humans we know that autoantibodies are common and, alas, also that the second postulate is unethical and the third controversial. In reality, a disease is considered autoimmune when target organ destruction is allied to the presence of disease-specific target organ autoantibodies (2). It is through their clinical phenotype that diseases gain identity; only recently have we used genetic and immune responses to adapt disease names. Therefore, the historical characteristic of severe diabetes as childhood-onset disease was supplanted by insulin-dependent diabetes and with identification of diabetes-associated autoantibodies and genetic susceptibility through the major histocompatibilty complex (MHC) for type 1 diabetes, or more precisely type 1a diabetes, with type 2 diabetes being everything type 1 diabetes was not (2,3).

From the earliest years it was …

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