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


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
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 Abiru, N.
Right arrow Articles by Eisenbarth, G. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Abiru, N.
Right arrow Articles by Eisenbarth, G. S.
Social Bookmarking
Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
Diabetes 50:1274-1281, 2001
© 2001 by the American Diabetes Association, Inc.

Peptide and Major Histocompatibility Complex–Specific Breaking of Humoral Tolerance to Native Insulin With the B9-23 Peptide in Diabetes-Prone and Normal Mice

Norio Abiru, Aristides K. Maniatis, Liping Yu, Dongmei Miao, Hiroaki Moriyama, Dale Wegmann, and George S. Eisenbarth

Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Denver, Colorado

NOD mice spontaneously develop anti-insulin autoantibodies and diabetes. A dominant peptide recognized by T-cell clones from NOD mice is insulin B-chain peptide B9-23. When administered subcutaneously to NOD mice, this peptide decreases the development of diabetes. In this study, we evaluated the autoantibody response to native insulin after administration of the B9-23 peptide. In NOD mice, administration of the B9-23 peptide in incomplete Freund’s adjuvant enhanced their insulin autoantibody response with a higher level and longer persistence. Induction of insulin autoantibodies with the B9-23 peptide was observed in non–diabetes-prone BALB/c mice and NOR mice within 2 weeks of administration, but this was not observed in C57BL/6 mice. A series of A-chain, other B-chain, and proinsulin peptides did not induce insulin autoantibodies. Induced anti-insulin autoantibodies could not be absorbed with the peptide alone but could be absorbed with native insulin. The B13-23 peptide (one of two identified epitopes within B9-23) when administered to BALB/c mice, induced autoantibodies, whereas peptide B9-16 did not. Induction of autoantibodies mapped to the major histocompatibility complex (MHC) rather than to the background genes. Both splenocytes with I-Ad/I-Ed or I-Ag7/I-Enull presented the B9-23 peptide to NOD islet-derived T-cell clones. Finally, administration of the B9-23 peptide to BALB/c mice, even without adjuvant, could induce insulin autoantibodies. Our results indicate that B-cell tolerance to intact insulin is readily broken with the presentation of the B9-23 insulin peptide, depending on the host’s specific MHC.


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
 J. Immunol.Home page
M. Kobayashi, N. Abiru, T. Arakawa, K. Fukushima, H. Zhou, E. Kawasaki, H. Yamasaki, E. Liu, D. Miao, F. S. Wong, et al.
Altered B:9 23 Insulin, When Administered Intranasally with Cholera Toxin Adjuvant, Suppresses the Expression of Insulin Autoantibodies and Prevents Diabetes
J. Immunol., August 15, 2007; 179(4): 2082 - 2088.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
C.-Q. Xia, R. Peng, Y. Qiu, M. Annamalai, D. Gordon, and M. J. Clare-Salzler
Transfusion of Apoptotic {beta}-Cells Induces Immune Tolerance to {beta}-Cell Antigens and Prevents Type 1 Diabetes in NOD Mice
Diabetes, August 1, 2007; 56(8): 2116 - 2123.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
J. M. Jasinski, L. Yu, M. Nakayama, M. M. Li, M. A. Lipes, G. S. Eisenbarth, and E. Liu
Transgenic Insulin (B:9-23) T-Cell Receptor Mice Develop Autoimmune Diabetes Dependent Upon RAG Genotype, H-2g7 Homozygosity, and Insulin 2 Gene Knockout.
Diabetes, July 1, 2006; 55(7): 1978 - 1984.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
D. Devendra, J. Jasinski, E. Melanitou, M. Nakayama, M. Li, B. Hensley, J. Paronen, H. Moriyama, D. Miao, G. S. Eisenbarth, et al.
Interferon-{alpha} as a Mediator of Polyinosinic:Polycytidylic Acid-Induced Type 1 Diabetes
Diabetes, September 1, 2005; 54(9): 2549 - 2556.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
H. Moriyama, N. Abiru, J. Paronen, K. Sikora, E. Liu, D. Miao, D. Devendra, J. Beilke, R. Gianani, R. G. Gill, et al.
Evidence for a primary islet autoantigen (preproinsulin 1) for insulitis and diabetes in the nonobese diabetic mouse
PNAS, September 2, 2003; 100(18): 10376 - 10381.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
H. Moriyama, L. Wen, N. Abiru, E. Liu, L. Yu, D. Miao, R. Gianani, F. S. Wong, and G. S. Eisenbarth
Induction and acceleration of insulitis/diabetes in mice with a viral mimic (polyinosinic-polycytidylic acid) and an insulin self-peptide
PNAS, April 16, 2002; 99(8): 5539 - 5544.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
H. Moriyama, L. Wen, N. Abiru, E. Liu, L. Yu, D. Miao, R. Gianani, F. S. Wong, and G. S. Eisenbarth
Induction and acceleration of insulitis/diabetes in mice with a viral mimic (polyinosinic-polycytidylic acid) and an insulin self-peptide
PNAS, April 16, 2002; 99(8): 5539 - 5544.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 2001 by the American Diabetes Association.