Autoimmune Inflammation and Insulin Resistance: Hallmarks So Far and Yet So Close to Explain Diabetes Endotypes.
Adipose tissue
Autoimmune inflammation
Autoreactive T cells
Diabetes endotypes
Insulin resistance
Journal
Current diabetes reports
ISSN: 1539-0829
Titre abrégé: Curr Diab Rep
Pays: United States
ID NLM: 101093791
Informations de publication
Date de publication:
13 12 2021
13 12 2021
Historique:
accepted:
03
10
2021
entrez:
13
12
2021
pubmed:
14
12
2021
medline:
29
1
2022
Statut:
epublish
Résumé
Diabetes mellitus can be categorized into two major variants, type 1 and type 2. A number of traits such as clinical phenotype, age at disease onset, genetic background, and underlying pathogenesis distinguish the two forms. Recent evidence indicates that type 1 diabetes can be accompanied by insulin resistance and type 2 diabetes exhibits self-reactivity. These two previously unknown conditions can influence the progression and outcome of the disease. Unlike most conventional considerations, diabetes appears to consist of a spectrum of intermediate phenotypes that includes monogenic and polygenic loci linked to inflammatory processes including autoimmunity, beta cell impairment, and insulin resistance. Here we discuss why a shift of the classical bi-modal view of diabetes (autoimmune vs. non-autoimmune) is necessary in favor of a model of an immunological continuum of endotypes lying between the two extreme "insulin-resistant" and "autoimmune beta cell targeting," shaped by environmental and genetic factors which contribute to determine specific immune-conditioned outcomes.
Identifiants
pubmed: 34902055
doi: 10.1007/s11892-021-01430-3
pii: 10.1007/s11892-021-01430-3
pmc: PMC8668851
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
54Subventions
Organisme : Juvenile Diabetes Research Foundation United States of America
ID : 3-APF-2019-744-A-N to AP
Informations de copyright
© 2021. The Author(s).
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