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Immune therapy in type 1 diabetes mellitus.

Lernmark, Åke LU orcid and Larsson, Helena LU orcid (2013) In Nature Reviews Endocrinology 9(2). p.92-103
Abstract
Type 1 diabetes mellitus (T1DM) is an autoimmune disorder directed against the β cells of the pancreatic islets. The genetic risk of the disease is linked to HLA-DQ risk alleles and unknown environmental triggers. In most countries, only 10-15% of children or young adults newly diagnosed with T1DM have a first-degree relative with the disease. Autoantibodies against insulin, GAD65, IA-2 or the ZnT8 transporter mark islet autoimmunity. These islet autoantibodies may already have developed in children of 1-3 years of age. Immune therapy in T1DM is approached at three different stages. Primary prevention is treatment of individuals at increased genetic risk. For example, one trial is testing if hydrolyzed casein milk formula reduces T1DM... (More)
Type 1 diabetes mellitus (T1DM) is an autoimmune disorder directed against the β cells of the pancreatic islets. The genetic risk of the disease is linked to HLA-DQ risk alleles and unknown environmental triggers. In most countries, only 10-15% of children or young adults newly diagnosed with T1DM have a first-degree relative with the disease. Autoantibodies against insulin, GAD65, IA-2 or the ZnT8 transporter mark islet autoimmunity. These islet autoantibodies may already have developed in children of 1-3 years of age. Immune therapy in T1DM is approached at three different stages. Primary prevention is treatment of individuals at increased genetic risk. For example, one trial is testing if hydrolyzed casein milk formula reduces T1DM incidence in genetically predisposed infants. Secondary prevention is targeted at individuals with persistent islet autoantibodies. Ongoing trials involve nonautoantigen-specific therapies, such as Bacillus Calmette-Guérin vaccine or anti-CD3 monoclonal antibodies, or autoantigen-specific therapies, including oral and nasal insulin or alum-formulated recombinant human GAD65. Trial interventions at onset of T1DM have also included nonautoantigen-specific approaches, and autoantigen-specific therapies, such as proinsulin peptides. Although long-term preservation of β-cell function has been difficult to achieve in many studies, considerable progress is being made through controlled clinical trials and animal investigations towards uncovering mechanisms of β-cell destruction. Novel therapies that prevent islet autoimmunity or halt progressive β-cell destruction are needed. (Less)
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author
and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Nature Reviews Endocrinology
volume
9
issue
2
pages
92 - 103
publisher
Nature Publishing Group
external identifiers
  • wos:000314738900008
  • pmid:23296174
  • scopus:84872853977
  • pmid:23296174
ISSN
1759-5037
DOI
10.1038/nrendo.2012.237
language
English
LU publication?
yes
id
9e75a142-756c-466f-83ec-d4bb16df7f68 (old id 3438954)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/23296174?dopt=Abstract
date added to LUP
2016-04-01 11:10:29
date last changed
2024-10-07 22:54:30
@article{9e75a142-756c-466f-83ec-d4bb16df7f68,
  abstract     = {{Type 1 diabetes mellitus (T1DM) is an autoimmune disorder directed against the β cells of the pancreatic islets. The genetic risk of the disease is linked to HLA-DQ risk alleles and unknown environmental triggers. In most countries, only 10-15% of children or young adults newly diagnosed with T1DM have a first-degree relative with the disease. Autoantibodies against insulin, GAD65, IA-2 or the ZnT8 transporter mark islet autoimmunity. These islet autoantibodies may already have developed in children of 1-3 years of age. Immune therapy in T1DM is approached at three different stages. Primary prevention is treatment of individuals at increased genetic risk. For example, one trial is testing if hydrolyzed casein milk formula reduces T1DM incidence in genetically predisposed infants. Secondary prevention is targeted at individuals with persistent islet autoantibodies. Ongoing trials involve nonautoantigen-specific therapies, such as Bacillus Calmette-Guérin vaccine or anti-CD3 monoclonal antibodies, or autoantigen-specific therapies, including oral and nasal insulin or alum-formulated recombinant human GAD65. Trial interventions at onset of T1DM have also included nonautoantigen-specific approaches, and autoantigen-specific therapies, such as proinsulin peptides. Although long-term preservation of β-cell function has been difficult to achieve in many studies, considerable progress is being made through controlled clinical trials and animal investigations towards uncovering mechanisms of β-cell destruction. Novel therapies that prevent islet autoimmunity or halt progressive β-cell destruction are needed.}},
  author       = {{Lernmark, Åke and Larsson, Helena}},
  issn         = {{1759-5037}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{92--103}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Nature Reviews Endocrinology}},
  title        = {{Immune therapy in type 1 diabetes mellitus.}},
  url          = {{https://lup.lub.lu.se/search/files/2438824/3864044.pdf}},
  doi          = {{10.1038/nrendo.2012.237}},
  volume       = {{9}},
  year         = {{2013}},
}