NYAS Conferences
New York Academy of Sciences
left end
Search
divider divider feedback right end
Annals of the New York Academy of Sciences Annals of the New York Academy of Sciences login

Main

Browse Volumes

Forthcoming Volumes

Annals PrePrints

Annals Extra

E-mail Alerts

Subscriptions & Orders

New Proposals

Author Guidelines

About Annals

Help

Get free Annals volume as a NYAS member: http://www.nyas.org/annalsreaderhw
Issue 1103 coverHow Do We Best Employ Animal Models for Type 1 Diabetes and Multiple Sclerosis? Volume 1103 published April 2007
Ann. N.Y. Acad. Sci. 1103: 77–89 (2007). doi: 10.1196/annals.1394.002
Copyright © 2007 by the New York Academy of Sciences
description | purchase volume purchase this volume

This Volume
Table of Contents
Description
This Article
Full Text
Full Text (PDF)
All Versions of this Article:
annals.1394.002v1
1103/1/77    most recent
Services
Similar articles in this journal
Similar articles in PubMed
Alert me to new issues of the journal
Download to citation manager
Citing Articles
Citing Articles via HighWire
Citing Articles via Google Scholar
Google Scholar
Articles by SHULTZ, L. D.
Articles by GREINER, D. L.
Search for Related Content
PubMed
PubMed Citation
Articles by SHULTZ, L. D.
Articles by GREINER, D. L.

Humanized, Transgenic, or Congenic Models

Humanized NOD/LtSz-scid IL2 Receptor Common Gamma Chain Knockout Mice in Diabetes Research

LEONARD D. SHULTZa, TODD PEARSONb, MARIE KINGb, LISA GIASSIb, LISA CARNEYa, BRUCE GOTTa, BONNIE LYONSa, ALDO A. ROSSINIb AND DALE L. GREINERb

a Jackson Laboratory, Bar Harbor, Maine, USA b Division of Diabetes, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA

Key Words: humanized mice • NOD-scid IL2r{gamma}null • diabetes • immunodeficient mice

Address for correspondence: Dr. Dale L. Greiner, Division of Diabetes, Department of Medicine, 373 Plantation Street, Biotech 2, Suite 218, Worcester, MA 01605. Voice: 508-856-3800; fax: 508-856-4093.  dale.greiner{at}umassmed.edu

There are many rodent models of autoimmune diabetes that have been used to study the pathogenesis of human type 1 diabetes (T1D), including the non-obese diabetic (NOD) mouse, the biobreeding (BB) rat, and the transgenic mouse models. However, mice and rats are not humans, and these rodent models do not completely recapitulate the autoimmune pathogenesis of the human disease. In addition, many of the reagents, tools, and therapeutics proposed for use in humans may be species specific and cannot be investigated in rodents. Researchers have used nonhuman primates to more closely mimic the human immune system and, to study species-specific therapeutics, but these studies are associated with additional ethical and economic constraints and, to date, no model of autoimmune diabetes in this species has been described. New animal models are needed that will permit the in vivo investigation of human immune systems and analyses of the pathogenesis of human T1D without putting individuals at risk. To fill this need, we are developing humanized mouse models for the in vivo study of T1D. These models are based on our newly generated stock of NOD-scid IL2r{gamma}null mice, which engraft at higher levels with human hematolymphoid cells and exhibit enhanced function of the engrafted human immune systems compared with previous humanized mouse models. Overall, development of these new generations of humanized mice should facilitate in vivo studies of the human immune system as well as permit the investigation of the pathogenesis and effector phases of human T1D.




This article has been cited by other articles:


Home page
DiabetesHome page
G. Fousteri and M. von Herrath
First-Trimester Human Fetal Pancreas Transplantation for Type 1 Diabetes Treatment: An Alternative Approach for Achieving Long-Term Graft Survival?
Diabetes, March 1, 2008; 57(3): 525 - 526.
[Full Text] [PDF]



footerLeft footerRight