JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
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
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 arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Huber, S. A.
Right arrow Articles by Newell, M. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Huber, S. A.
Right arrow Articles by Newell, M. K.

 Previous Article  |  Next Article 

Journal of Virology, July 1999, p. 5630-5636, Vol. 73, No. 7
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

gamma delta + T Cells Regulate Major Histocompatibility Complex Class II (IA and IE)-Dependent Susceptibility to Coxsackievirus B3-Induced Autoimmune Myocarditis

S. A. Huber,1,* J. E. Stone,2 D. H. Wagner Jr.,3 J. Kupperman,2 L. Pfeiffer,4 C. David,5 R. L. O'Brien,3 G. S. Davis,4 and M. K. Newell2

Department of Pathology1 and Immunobiology Program2 and Pulmonary Disease and Critical Care Unit,4 Department of Medicine, University of Vermont College of Medicine, Burlington, Vermont 05405; National Jewish Medical Research Center, Denver, Colorado 80206, and Department of Immunology, University of Colorado Health Sciences Center, Denver, Colorado 802623; and Department of Immunology, Mayo Clinic, Rochester, Minnesota 559055

Received 29 January 1999/Accepted 6 April 1999

Coxsackievirus B3 (CVB3) infection induces myocardial inflammation and myocyte necrosis in some, but not all, strains of mice. C57BL/6 mice, which inherently lack major histocompatibility complex (MHC) class II IE antigen, develop minimal cardiac lesions despite high levels of virus in the heart. The present experiments evaluate the relative roles of class II IA and IE expression on myocarditis susceptibility in four transgenic C57BL/6 mouse strains differing in MHC class II antigen expression. Animals lacking MHC class II IE antigen (C57BL/6 [IA+ IE-] and ABo [IA- IE-]) developed minimal cardiac lesions subsequent to infection despite high concentrations of virus in the heart. In contrast, strains expressing IE (ABo Ealpha [IA- IE+] and Bl.Tg.Ealpha [IA+ IE+]) had substantial cardiac injury. Myocarditis susceptibility correlated to a Th1 (gamma interferon-positive) cell response in the spleen, while disease resistance correlated to a preferential Th2 (interleukin-4-positive) phenotype. Vgamma /Vdelta analysis indicates that distinct subpopulations of gamma delta + T cells are activated after CVB3 infection of C57BL/6 and Bl.Tg.Ealpha mice. Depletion of gamma delta + T cells abrogated myocarditis susceptibility in IE+ animals and resulted in a Th1right-arrowTh2 phenotype shift. These studies indicate that the MHC class II antigen haplotype controls myocarditis susceptibility, that this control is most likely mediated through the type of gamma delta T cells activated during CVB3 infection, and finally that different subpopulations of gamma delta + T cells may either promote or inhibit Th1 cell responses.

* Corresponding author. Mailing address: Department of Pathology, University of Vermont, 55A South Park Dr., Colchester, VT 05446. Phone: (802) 656-8944. Fax: (802) 656-8965. E-mail: shuber{at}salus.med.uvm.edu.

Journal of Virology, July 1999, p. 5630-5636, Vol. 73, No. 7
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 1999 by the American Society for Microbiology. All rights reserved.