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Type 1 Diabetes

Jönsson, Josefine LU orcid and Lernmark, Ake LU orcid (2025) p.12-23
Abstract
Type 1 diabetes, formerly known as juvenile diabetes or insulin-dependent diabetes, results from the specific autoimmune destruction of the pancreatic islet beta cells. The subsequent loss of insulin leads to increased blood and urine glucose. The classical symptoms are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss. The disease may be diagnosed at any age but only in individuals with certain HLA-DR-DQ-susceptibility haplotypes. Several non-HLA genetic factors either contribute to the genetic etiology or the progression toward the clinical onset of the disease. Standardized tests for autoantibodies against either insulin (IAA) or GAD65 (GADA) have made it possible to demonstrate... (More)
Type 1 diabetes, formerly known as juvenile diabetes or insulin-dependent diabetes, results from the specific autoimmune destruction of the pancreatic islet beta cells. The subsequent loss of insulin leads to increased blood and urine glucose. The classical symptoms are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss. The disease may be diagnosed at any age but only in individuals with certain HLA-DR-DQ-susceptibility haplotypes. Several non-HLA genetic factors either contribute to the genetic etiology or the progression toward the clinical onset of the disease. Standardized tests for autoantibodies against either insulin (IAA) or GAD65 (GADA) have made it possible to demonstrate that the disease is often triggered during the first years of life, earlier for IAA and later for GADA. Environmental factors such as viruses may trigger IAA and GADA, which appear in a way associated with human leukocyte antigen (HLA). Individuals who have developed IAA, GADA, or both may develop yet other autoantibodies against IA-2 (IA-2A), ZnT8 transporter (ZnT8A), or both. Individuals with two or more islet autoantibodies will go on to develop type 1 diabetes (100%), but it may take 20 years. Persistent single autoantibody positive individuals are at reduced risk (15%) over 20 years. The pathogenesis is likely controlled by CD8+ T cells recognizing autoantigen–peptides on HLA class I proteins expressed on the beta cell surface. Autoantibodies may contribute to the beta cell toxicity. The progression toward clinical onset is associated with a loss of beta cells in parallel to slowly increasing HbA1c within the normal range. The disease is predictable through HLA typing, including non-HLA genes in a Genetic Risk Score (GRS) and tests of IAA, GADA, IA-2A, and ZnT8A. Prevention and intervention trials aim to halt the beta cell–autoimmune process, but the results of these trials have not altered how patients with type 1 diabetes are treated. (Less)
Please use this url to cite or link to this publication:
author
and
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
epub
subject
host publication
Encyclopedia of Immunobiology
editor
Kaye, Paul M.
edition
2
pages
12 - 23
publisher
Elsevier
ISBN
978-0-12-824480-7
DOI
10.1016/B978-0-12-824465-4.00176-9
language
English
LU publication?
yes
id
55b23d9a-14f3-4a75-83bf-bbe7ead2655c
date added to LUP
2025-10-17 07:23:24
date last changed
2025-10-17 07:23:24
@inbook{55b23d9a-14f3-4a75-83bf-bbe7ead2655c,
  abstract     = {{Type 1 diabetes, formerly known as juvenile diabetes or insulin-dependent diabetes, results from the specific autoimmune destruction of the pancreatic islet beta cells. The subsequent loss of insulin leads to increased blood and urine glucose. The classical symptoms are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss. The disease may be diagnosed at any age but only in individuals with certain HLA-DR-DQ-susceptibility haplotypes. Several non-HLA genetic factors either contribute to the genetic etiology or the progression toward the clinical onset of the disease. Standardized tests for autoantibodies against either insulin (IAA) or GAD65 (GADA) have made it possible to demonstrate that the disease is often triggered during the first years of life, earlier for IAA and later for GADA. Environmental factors such as viruses may trigger IAA and GADA, which appear in a way associated with human leukocyte antigen (HLA). Individuals who have developed IAA, GADA, or both may develop yet other autoantibodies against IA-2 (IA-2A), ZnT8 transporter (ZnT8A), or both. Individuals with two or more islet autoantibodies will go on to develop type 1 diabetes (100%), but it may take 20 years. Persistent single autoantibody positive individuals are at reduced risk (15%) over 20 years. The pathogenesis is likely controlled by CD8+ T cells recognizing autoantigen–peptides on HLA class I proteins expressed on the beta cell surface. Autoantibodies may contribute to the beta cell toxicity. The progression toward clinical onset is associated with a loss of beta cells in parallel to slowly increasing HbA1c within the normal range. The disease is predictable through HLA typing, including non-HLA genes in a Genetic Risk Score (GRS) and tests of IAA, GADA, IA-2A, and ZnT8A. Prevention and intervention trials aim to halt the beta cell–autoimmune process, but the results of these trials have not altered how patients with type 1 diabetes are treated.}},
  author       = {{Jönsson, Josefine and Lernmark, Ake}},
  booktitle    = {{Encyclopedia of Immunobiology}},
  editor       = {{Kaye, Paul M.}},
  isbn         = {{978-0-12-824480-7}},
  language     = {{eng}},
  pages        = {{12--23}},
  publisher    = {{Elsevier}},
  title        = {{Type 1 Diabetes}},
  url          = {{http://dx.doi.org/10.1016/B978-0-12-824465-4.00176-9}},
  doi          = {{10.1016/B978-0-12-824465-4.00176-9}},
  year         = {{2025}},
}