The JI
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 Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
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 Chen, C.
Right arrow Articles by Liu, C.-P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chen, C.
Right arrow Articles by Liu, C.-P.
The Journal of Immunology, 2006, 176: 3449-3460.
Copyright © 2006 by The American Association of Immunologists

Regulatory T Cells Can Mediate Their Function through the Stimulation of APCs to Produce Immunosuppressive Nitric Oxide1

Cyndi Chen, Wen-hui Lee, Lingwen Zhong and Chih-Pin Liu2

Division of Immunology, Beckman Research Institute, City of Hope Duarte, CA 91010

Regulatory T cells (Tr cells) play a critical role in inducing immune tolerance. It remains largely unclear how various types of Tr cells perform their regulatory function. We have studied the underlying regulatory mechanism of a population of autoantigen-specific CD4+ Tr cells. These T cells are specific for the glutamic acid decarboxylase p206–220 peptide and are isolated from the diabetes-resistant nonobese-resistant mice. Although these T cells express T-bet and display a Th1 phenotype, they are able to inhibit diabetes. Their regulatory function is dependent on both IFN-{gamma} and cell contact with target cells. These Tr cells can mediate their cell contact-dependent regulatory function by secreting IFN-{gamma} which stimulates APCs to produce NO. NO is necessary for the Tr cells to inhibit the proliferation of pathogenic T cells and the development of diabetes. Therefore, we have identified a novel mechanism by which these Tr cells can exert their regulatory function. These results also provide an explanation as to why IFN-{gamma} may play both pathogenic and immunomodulatory roles in autoimmune diseases.




This article has been cited by other articles:


Home page
J. Leukoc. Biol.Home page
T. Kheradmand, P. P. Trivedi, N. A. Wolf, P. C. Roberts, and R. H. Swanborg
Characterization of a subset of bone marrow-derived natural killer cells that regulates T cell activation in rats
J. Leukoc. Biol., May 1, 2008; 83(5): 1128 - 1135.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
I. M. Irmler, M. Gajda, and R. Brauer
Exacerbation of Antigen-Induced Arthritis in IFN-{gamma}-Deficient Mice As a Result of Unrestricted IL-17 Response
J. Immunol., November 1, 2007; 179(9): 6228 - 6236.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
W. Badn, E. Visse, A. Darabi, K. E. Smith, L. G. Salford, and P. Siesjo
Postimmunization with IFN-{gamma}-Secreting Glioma Cells Combined with the Inducible Nitric Oxide Synthase Inhibitor Mercaptoethylguanidine Prolongs Survival of Rats with Intracerebral Tumors
J. Immunol., September 15, 2007; 179(6): 4231 - 4238.
[Abstract] [Full Text] [PDF]


Home page
Mol Hum ReprodHome page
A. van der Meer, H.G.M. Lukassen, B. van Cranenbroek, E.H. Weiss, D.D.M. Braat, M.J. van Lierop, and I. Joosten
Soluble HLA-G promotes Th1-type cytokine production by cytokine-activated uterine and peripheral natural killer cells
Mol. Hum. Reprod., February 1, 2007; 13(2): 123 - 133.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 2006 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 2006 by The American Association of Immunologists, Inc. All rights reserved.