Diabetes
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Charlton, B.
Right arrow Articles by Mandel, T. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Charlton, B.
Right arrow Articles by Mandel, T. E.
Social Bookmarking
Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes, Vol 37, Issue 8 1108-1112, Copyright © 1988 by American Diabetes Association

ARTICLES

Progression from insulitis to beta-cell destruction in NOD mouse requires L3T4+ T-lymphocytes

B Charlton and TE Mandel
Transplantation Unit, Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Parkville, Victoria, Australia.

The identity of the cells responsible for beta-cell destruction in type I (insulin-dependent) diabetes is still uncertain. L3T4+ T-lymphocytes have a role in the initiation of insulitis and in damaging transplanted allogeneic islets in nonobese diabetic (NOD) mice. The role of L3T4+ T-lymphocytes in destruction of beta-cells of the NOD mouse was studied in cyclophosphamide (CY)-induced diabetic NOD mice with a rat anti-L3T4 monoclonal antibody (MoAb). After administration of CY, most untreated animals became diabetic, whereas all antibody-treated animals remained normoglycemic. Insulitis was still present in MoAb-treated animals, but immunocytochemical staining showed rat antibody blocking the L3T4 antigen on T-lymphocytes. This study provides further evidence that L3T4+ T-lymphocytes are critical to the process of beta-cell destruction in NOD mice. The means by which L3T4+ cells exert their effect remains to be clarified.
Add to CiteULike CiteULike   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 DiabetesHome page
A. Jorns, A. Gunther, H.-J. Hedrich, D. Wedekind, M. Tiedge, and S. Lenzen
Immune Cell Infiltration, Cytokine Expression, and {beta}-Cell Apoptosis During the Development of Type 1 Diabetes in the Spontaneously Diabetic LEW.1AR1/Ztm-iddm Rat
Diabetes, July 1, 2005; 54(7): 2041 - 2052.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
S. Ma, Y. Huang, Z. Yin, R. Menassa, J. E. Brandle, and A. M. Jevnikar
Induction of oral tolerance to prevent diabetes with transgenic plants requires glutamic acid decarboxylase (GAD) and IL-4
PNAS, April 13, 2004; 101(15): 5680 - 5685.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
H. E. Thomas, W. Irawaty, R. Darwiche, T. C. Brodnicki, P. Santamaria, J. Allison, and T. W.H. Kay
IL-1 Receptor Deficiency Slows Progression to Diabetes in the NOD Mouse
Diabetes, January 1, 2004; 53(1): 113 - 121.
[Abstract] [Full Text] [PDF]

Home page
 JEMHome page
D. Kagi, B. Odermatt, P. Seiler, R. M. Zinkernagel, T. W. Mak, and H. Hengartner
Reduced Incidence and Delayed Onset of Diabetes in Perforin-deficient Nonobese Diabetic Mice
J. Exp. Med., October 6, 1997; 186(7): 989 - 997.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 1988 by the American Diabetes Association.