Modeling human T1D-associated autoimmune processes.
Autoimmunity
Beta cell destruction
Disease modeling
Humanized mice
In vitro models
Type 1 diabetes
Journal
Molecular metabolism
ISSN: 2212-8778
Titre abrégé: Mol Metab
Pays: Germany
ID NLM: 101605730
Informations de publication
Date de publication:
02 2022
02 2022
Historique:
received:
27
09
2021
revised:
19
11
2021
accepted:
07
12
2021
pubmed:
14
12
2021
medline:
5
4
2022
entrez:
13
12
2021
Statut:
ppublish
Résumé
Type 1 diabetes (T1D) is an autoimmune disease characterized by impaired immune tolerance to β-cell antigens and progressive destruction of insulin-producing β-cells. Animal models have provided valuable insights for understanding the etiology and pathogenesis of this disease, but they fall short of reflecting the extensive heterogeneity of the disease in humans, which is contributed by various combinations of risk gene alleles and unique environmental factors. Collectively, these factors have been used to define subgroups of patients, termed endotypes, with distinct predominating disease characteristics. Here, we review the gaps filled by these models in understanding the intricate involvement and regulation of the immune system in human T1D pathogenesis. We describe the various models developed so far and the scientific questions that have been addressed using them. Finally, we discuss the limitations of these models, primarily ascribed to hosting a human immune system (HIS) in a xenogeneic recipient, and what remains to be done to improve their physiological relevance. To understand the role of genetic and environmental factors or evaluate immune-modifying therapies in humans, it is critical to develop and apply models in which human cells can be manipulated and their functions studied under conditions that recapitulate as closely as possible the physiological conditions of the human body. While microphysiological systems and living tissue slices provide some of these conditions, HIS mice enable more extensive analyses using in vivo systems.
Sections du résumé
BACKGROUND
Type 1 diabetes (T1D) is an autoimmune disease characterized by impaired immune tolerance to β-cell antigens and progressive destruction of insulin-producing β-cells. Animal models have provided valuable insights for understanding the etiology and pathogenesis of this disease, but they fall short of reflecting the extensive heterogeneity of the disease in humans, which is contributed by various combinations of risk gene alleles and unique environmental factors. Collectively, these factors have been used to define subgroups of patients, termed endotypes, with distinct predominating disease characteristics.
SCOPE OF REVIEW
Here, we review the gaps filled by these models in understanding the intricate involvement and regulation of the immune system in human T1D pathogenesis. We describe the various models developed so far and the scientific questions that have been addressed using them. Finally, we discuss the limitations of these models, primarily ascribed to hosting a human immune system (HIS) in a xenogeneic recipient, and what remains to be done to improve their physiological relevance.
MAJOR CONCLUSIONS
To understand the role of genetic and environmental factors or evaluate immune-modifying therapies in humans, it is critical to develop and apply models in which human cells can be manipulated and their functions studied under conditions that recapitulate as closely as possible the physiological conditions of the human body. While microphysiological systems and living tissue slices provide some of these conditions, HIS mice enable more extensive analyses using in vivo systems.
Identifiants
pubmed: 34902607
pii: S2212-8778(21)00275-1
doi: 10.1016/j.molmet.2021.101417
pmc: PMC8739876
pii:
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
101417Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK103585
Pays : United States
Organisme : NIDDK NIH HHS
ID : UC4 DK104207
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI132963
Pays : United States
Organisme : NIDDK NIH HHS
ID : F31 DK121377
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001453
Pays : United States
Organisme : NIH HHS
ID : R24 OD026440
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI146828
Pays : United States
Organisme : NCATS NIH HHS
ID : TL1 TR001875
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK123559
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK107383
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK104218
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI142428
Pays : United States
Organisme : NIDDK NIH HHS
ID : U24 DK104162
Pays : United States
Informations de copyright
Copyright © 2021 The Author(s). Published by Elsevier GmbH.. All rights reserved.
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