The DOI matches its Crossref record; 119 of the 120 references it cites were found in a registry or an index.
Etiology of Type 1 Diabetes
Open accessAbstract
Recent genetic mapping and gene-phenotype studies have revealed the genetic architecture of type 1 diabetes. At least ten genes so far can be singled out as strong causal candidates. The known functions of these genes indicate the primary etiological pathways of this disease, including HLA class II and I molecules binding to preproinsulin peptides and T cell receptors, T and B cell activation, innate pathogen-viral responses, chemokine and cytokine signaling, and T regulatory and antigen-presenting cell functions. This review considers research in the field of type 1 diabetes toward identifying disease mechanisms using genetic approaches. The expression and functions of these pathways, and, therefore, disease susceptibility, will be influenced by epigenetic and environmental factors. Certain inherited immune phenotypes will be early precursors of type 1 diabetes and could be useful in future clinical trials.
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“Type 1 diabetes is generally thought to be precipitated by an immune-associated, if not directly immune-mediated, destruction of insulin-producing pancreatic β cells.1,2”
From Type 1 diabetes (2014) · cites this paper as [1]
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CTLA-4 Control over Foxp3 + Regulatory T Cell Function
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Self-citationNew genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk
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Self-citationGenetic variants regulating ORMDL3 expression contribute to the risk of childhood asthma
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Atkinson, M. A., Eisenbarth, G. S., & Michels, A. W. (2014) · The Lancet · doi:10.1016/s0140-6736(13)60591-7 · Cited by 2,931
Diabetes mellitus: The epidemic of the century
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Variation in the Human Immune System Is Largely Driven by Non-Heritable Influences
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Signaling and Function of Interleukin-2 in T Lymphocytes
Ross, S. H., & Cantrell, D. A. (2018) · Annual Review of Immunology · doi:10.1146/annurev-immunol-042617-053352 · Cited by 1,025
Metadata
- Authors
- Todd, J. A.
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- Todd, John A.
- ORCID
- Todd, John A.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2010-04
- Volume
- 32
- Issue
- 4
- Pages
- 457-467
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W1997112242
- Cited by
- 560
- References
- 120
- Citations by year
- 2026: 12 · 2025: 19 · 2024: 30 · 2023: 32 · 2022: 28 · 2021: 32 · 2020: 35 · 2019: 29 · 2018: 25 · 2017: 22 · 2016: 47 · 2015: 49 · 2014: 45 · 2013: 38 · 2012: 59
- FWCI
- 5.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust (061858)
- National Institute for Health and Care Research (NF-SI-0508-10275)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- type 1 diabetes, genetic etiology, HLA class II, HLA class I, T cell receptor, T cell activation, B cell activation, innate immune response, viral infection, chemokine signaling, cytokine signaling, regulatory T cells, antigen-presenting cells, epigenetic factors, environmental factors, disease susceptibility, gene mapping, genotype-phenotype correlation
- MeSH terms
- Animals, Diabetes Mellitus, Type 1, Gene Expression Regulation, Humans, Phenotype, Genetic Predisposition to Disease, Epigenesis, Genetic
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