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Journal of Virology, November 2002, p. 10785-10790, Vol. 76, No. 21
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.21.10785-10790.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

V{gamma}4+ T Cells Promote Autoimmune CD8+ Cytolytic T-Lymphocyte Activation in Coxsackievirus B3-Induced Myocarditis in Mice: Role for CD4+ Th1 Cells

S. A. Huber,1* D. Sartini,1 and M. Exley2

Department of Pathology, University of Vermont, Burlington, Vermont,1 Beth Israel Deaconess Medical Center, Boston, Massachusetts2

Received 17 May 2002/ Accepted 5 August 2002

T cells expressing the V{gamma}4 T-cell receptor (TCR) promote myocarditis in coxsackievirus B3 (CVB3)-infected BALB/c mice. CD1, a major histocompatibility complex (MHC) class I-like molecule, is required for activation of V{gamma}4+ cells. Once activated, V{gamma}4+ cells initiate myocarditis through gamma interferon (IFN-{gamma})-mediated induction of CD4+ T helper type 1 (Th1) cells in the infected animal. These CD4+ Th1 cells are required for activation of an autoimmune CD8+ {alpha}ß TCR+ effector, which is the predominant pathogenic agent in this model of CVB3-induced myocarditis. Activated V{gamma}4+ cells can adoptively transfer myocarditis into BALB/c mice infected with a nonmyocarditic variant of CVB3 (H310A1) but cannot transfer myocarditis into either uninfected or CD1-/- recipients, demonstrating the need for both infection and CD1 expression for V{gamma}4+ cell function. In contrast, CD8+ {alpha}ß TCR+ cells transfer myocarditis into either infected CD1-/- or uninfected recipients, showing that once activated, the CD8+ {alpha}ß TCR+ effectors function independently of both virus and CD1. V{gamma}4+ cells given to mice lacking CD4+ T cells minimally activate the CD8+ {alpha}ß TCR+ cells. These studies show that V{gamma}4+ cells determine CVB3 pathogenicity by their ability to influence both the CD4+ and CD8+ adaptive immune response. V{gamma}4+ cells enhance CD4+ Th1 (IFN-{gamma}+) cell activation through IFN-{gamma}- and CD1-dependent mechanisms. CD4+ Th1 cells promote activation of the autoimmune CD8+ {alpha}ß TCR+ effectors.

* Corresponding author. Mailing address: University of Vermont, Department of Pathology, 208 S. Park Drive, Suite 2, Colchester, VT 05446. Phone: (802) 656-8944. Fax: (802) 656-8965. E-mail: Sally.Huber{at}uvm.edu.

Journal of Virology, November 2002, p. 10785-10790, Vol. 76, No. 21
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.21.10785-10790.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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