HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Chen, C. Articles by Liu, C.-P. Search for Related Content PubMed PubMed Citation Articles by Chen, C. Articles by Liu, C.-P.

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

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- and cell contact with target cells. These Tr cells can mediate their cell contact-dependent regulatory function by secreting IFN- 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- may play both pathogenic and immunomodulatory roles in autoimmune diseases.

This article has been cited by other articles:

				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]

				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]

				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]

				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]