Immune intervention in type 1 diabetes
Open accessAbstract
Type 1 diabetes (T1D) is a chronic autoimmune disease that results in the specific immune destruction of insulin producing beta cells. Currently there is no cure for T1D and treatment for the disease consists of lifelong administration of insulin. Immunotherapies aimed at preventing beta cell destruction in T1D patients with residual c-peptide or in individuals developing T1D are being evaluated. Networks of researchers such as TrialNet and the Immune Tolerance Network in the U.S. and similar networks in Europe have been established to evaluate such immunotherapies. This review focuses on immune intervention for the prevention and amelioration of human T1D with a focus on potential immune suppressive, antigen specific and environmental therapies.
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In patients with type 1 diabetes with surviving β cells, insulitic lesions are usually lobular, analogous to the lobular loss of melanocytes in vitiligo.
“In patients with type 1 diabetes with surviving β cells, insulitic lesions are usually lobular, analogous to the lobular loss of melanocytes in vitiligo.60”
From Type 1 diabetes (2014) · cites this paper as [60]
The Introduction (page unavailable) describes lobular β-cell destruction in patients with residual β cells, with normal-appearing islets beside areas lacking β cells. It does not describe insulitic lesions as usually lobular; it says insulitis is minimal in the great majority of pancreases examined at or after onset. Our copy also does not make the comparison with melanocyte loss in vitiligo. (LLM, conf=0.86)
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Cites
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“Those patients (and presumably prediabetic autoantibody positive individuals) have lobular destruction of islet beta cells with areas with “normal appearing” islets interspersed with areas where all islets contain only non-beta cells (termed pseudoatrophic islets) [21,22].”
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Cited by
Sorted by citations
Atkinson, M. A., Eisenbarth, G. S., & Michels, A. W. (2014) · The Lancet · doi:10.1016/s0140-6736(13)60591-7 · Cited by 2,713 · see citing works
Self-citation
- Authors
- Michels, A. W., & Eisenbarth, G. S.
- Affiliations
- University of Colorado Denver (US)
- ORCID
- Michels, Aaron W.
- Venue
- Seminars in Immunology
- Publisher
- Elsevier BV
- Published
- 2011-06
- Volume
- 23
- Issue
- 3
- Pages
- 214-219
- ISSN
- 1044-5323 (ISSN-L)
- PMC
- PMC3177994
- OpenAlex
- W2074214836
- Cited by
- 47
- References
- 14
- Citations by year
- 2025: 2 · 2024: 1 · 2022: 1 · 2020: 2 · 2019: 2 · 2018: 3 · 2017: 2 · 2016: 2 · 2015: 6 · 2014: 5 · 2013: 9 · 2012: 12
- FWCI
- 0.88
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Seminars in Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (U519 AI050864-08, U19AI050864)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK057516, R01DK055969, K08DK095995)
- 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, immunotherapy, beta cell destruction, autoimmune disease, immune tolerance, antigen-specific immunotherapy, immunosuppression, environmental therapy, TrialNet
- MeSH terms
- Animals, Antigens, Diabetes Mellitus, Type 1, Dietary Proteins, Humans, Immune Tolerance, Immunosuppression Therapy, Autoimmunity
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