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Foxp3(+) Regulatory T Cells in Mouse Models of Type 1 Diabetes

Studies on human type 1 diabetes (T1D) are facilitated by the availability of animal models such as nonobese diabetic (NOD) mice that spontaneously develop autoimmune diabetes, as well as a variety of genetically engineered mouse models with reduced genetic and pathogenic complexity, as compared to...

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Detalles Bibliográficos
Autores principales: Petzold, Cathleen, Riewaldt, Julia, Watts, Deepika, Sparwasser, Tim, Schallenberg, Sonja, Kretschmer, Karsten
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3647588/
https://www.ncbi.nlm.nih.gov/pubmed/23691523
http://dx.doi.org/10.1155/2013/940710
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author Petzold, Cathleen
Riewaldt, Julia
Watts, Deepika
Sparwasser, Tim
Schallenberg, Sonja
Kretschmer, Karsten
author_facet Petzold, Cathleen
Riewaldt, Julia
Watts, Deepika
Sparwasser, Tim
Schallenberg, Sonja
Kretschmer, Karsten
author_sort Petzold, Cathleen
collection PubMed
description Studies on human type 1 diabetes (T1D) are facilitated by the availability of animal models such as nonobese diabetic (NOD) mice that spontaneously develop autoimmune diabetes, as well as a variety of genetically engineered mouse models with reduced genetic and pathogenic complexity, as compared to the spontaneous NOD model. In recent years, increasing evidence has implicated CD4(+)CD25(+) regulatory T (Treg) cells expressing the transcription factor Foxp3 in both the breakdown of self-tolerance and the restoration of immune homeostasis in T1D. In this paper, we provide an overview of currently available mouse models to study the role of Foxp3(+) Treg cells in the control of destructive β cell autoimmunity, including a novel NOD model that allows specific and temporally controlled deletion of Foxp3(+) Treg cells.
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spelling pubmed-36475882013-05-20 Foxp3(+) Regulatory T Cells in Mouse Models of Type 1 Diabetes Petzold, Cathleen Riewaldt, Julia Watts, Deepika Sparwasser, Tim Schallenberg, Sonja Kretschmer, Karsten J Diabetes Res Review Article Studies on human type 1 diabetes (T1D) are facilitated by the availability of animal models such as nonobese diabetic (NOD) mice that spontaneously develop autoimmune diabetes, as well as a variety of genetically engineered mouse models with reduced genetic and pathogenic complexity, as compared to the spontaneous NOD model. In recent years, increasing evidence has implicated CD4(+)CD25(+) regulatory T (Treg) cells expressing the transcription factor Foxp3 in both the breakdown of self-tolerance and the restoration of immune homeostasis in T1D. In this paper, we provide an overview of currently available mouse models to study the role of Foxp3(+) Treg cells in the control of destructive β cell autoimmunity, including a novel NOD model that allows specific and temporally controlled deletion of Foxp3(+) Treg cells. Hindawi Publishing Corporation 2013 2013-03-14 /pmc/articles/PMC3647588/ /pubmed/23691523 http://dx.doi.org/10.1155/2013/940710 Text en Copyright © 2013 Cathleen Petzold et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Petzold, Cathleen
Riewaldt, Julia
Watts, Deepika
Sparwasser, Tim
Schallenberg, Sonja
Kretschmer, Karsten
Foxp3(+) Regulatory T Cells in Mouse Models of Type 1 Diabetes
title Foxp3(+) Regulatory T Cells in Mouse Models of Type 1 Diabetes
title_full Foxp3(+) Regulatory T Cells in Mouse Models of Type 1 Diabetes
title_fullStr Foxp3(+) Regulatory T Cells in Mouse Models of Type 1 Diabetes
title_full_unstemmed Foxp3(+) Regulatory T Cells in Mouse Models of Type 1 Diabetes
title_short Foxp3(+) Regulatory T Cells in Mouse Models of Type 1 Diabetes
title_sort foxp3(+) regulatory t cells in mouse models of type 1 diabetes
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3647588/
https://www.ncbi.nlm.nih.gov/pubmed/23691523
http://dx.doi.org/10.1155/2013/940710
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