The countdown to type 1 diabetes: when, how and why does the clock start?
Open accessAbstract
‘The clock to type 1 diabetes has started when islet antibodies are first detected’, commented George Eisenbarth with regard to the pathogenesis of type 1 diabetes. This review focuses on ‘starting the clock’, i.e. the initiation of pre-symptomatic islet autoimmunity/the first appearance of islet autoantibodies. In particular, this review addresses why susceptibility to developing islet autoimmunity is greatest in the first 2 years of life and why beta cells are a frequent target of the immune system during this fertile period. A concept for the development of beta cell autoimmunity in childhood is discussed and three factors are highlighted that contribute to this early predisposition: (1) high beta cell activity and potential vulnerability to stress; (2) high rates of and first exposures to infection; and (3) a heightened immune response, with a propensity for T helper type 1 (Th1) immunity. Arguments are presented that beta cell injury, accompanied by activation of an inflammatory immune response, precedes the initiation of autoimmunity. Finally, the implications for strategies aimed at primary prevention for a world without type 1 diabetes are discussed. Graphical Abstract
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Viral infections are associated with islet autoimmunity.
“Viral infections are associated with islet autoimmunity, 53”
From The future of type 1 diabetes therapy (2025) · cites this paper as [53]
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References 90 · Cited by 30
- Authors
- Ziegler, A.-G.
- Affiliations
- TUM Klinikum (DE)
- Corresponding author
- Ziegler, Anette-Gabriele
- Venue
- Diabetologia
- Published
- 2023-05-26
- Volume
- 66
- Issue
- 7
- Pages
- 1169-1178
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- PMC
- PMC10212739
- OpenAlex
- W4378348704
- Cited by
- 30
- References
- 90
- Citations by year
- 2026: 10 · 2025: 7 · 2024: 11 · 2023: 2
- FWCI
- 1.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Diabetologia (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion, cc-by)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion, other-oa)
- Funders
- LifeScience Stiftung (HMGU 2014.01, HMGU 2016.01)
- German Center for Diabetes Research
- Leona M. and Harry B. Helmsley Charitable Trust (718-Q-R)
- Bundesministerium für Bildung und Forschung (BMBF, grant FKZ01KX1818)
- Juvenile Diabetes Research Foundation United States of America (1-SRA-2014-310-M-R, 3-SRA-2015-72-M-R, 3-SRA-2019-)
- Helmholtz Zentrum München - Deutsches Forschungszentrum für Gesundheit und Umwelt (GmbH)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- type 1 diabetes, islet autoimmunity, islet autoantibodies, childhood, Th1 response, infection, beta-cell injury, inflammation, primary prevention, pathogenesis
- MeSH terms
- Autoantibodies, Diabetes Mellitus, Type 1, Female, Humans, Islets of Langerhans, Autoimmunity, Genetic Predisposition to Disease, Insulin-Secreting Cells
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