{'fraction_non_alphanumeric': 0.03230769230769231, 'fraction_numerical': 0.006153846153846154, 'mean_word_length': 5.259615384615385, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Etiology and pathogenesis of type I diabetes].

A large body of evidence supports the hypothesis that type I diabetes is an autoimmune disease. The development of type I diabetes can conceptually be divided in three stages: 1. genetic susceptibility, 2. pretype I diabetes with beginning beta-cell destruction and insulitis, and 3. clinical overt type I diabetes. During stage 2, an unknown "triggering event" leads to inflammation and active autoimmunity towards beta cells. In this chapter, recent developments concerning genetics and environmental factors, pathogenic mechanisms, prediction, and immunotherapy of type I diabetes will be reviewed.