| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Circulation, Vol 89, 2170-2175, Copyright © 1994 by American Heart Association
Y Seko, H Yagita, K Okumura and Y Yazaki
BACKGROUND: In viral myocarditis, we previously reported that natural
killer cells infiltrate the heart first, then activated T cells infiltrate
second and play an important role in the pathogenesis of the myocardial
damage. METHODS AND RESULTS: To elucidate the nature of T- cell
infiltration, using a murine model of acute myocarditis caused by
coxsackievirus B3, we analyzed the expression of T-cell receptor (TCR) V
beta genes in infiltrating cells in the heart by polymerase chain reaction
(PCR). The PCR-amplified products were confirmed by Southern blot
hybridization with a C beta cDNA probe. In contrast to spleen lymphocytes,
the repertoire of V beta gene transcripts in the heart was restricted. The
infiltrating cells expressing V beta 10 were found in six of eight hearts
of mice with acute myocarditis. The infiltrating cells expressing V beta 8
and V beta 13 were found in four of eight hearts with myocarditis,
respectively. Immunoperoxidase staining of serial sections of the heart of
myocarditis for TCR alpha beta chains and TCR V beta 10 confirmed that the
dominant population of infiltrating T cells expressed V beta 10 gene
products. CONCLUSIONS: The restricted usage of TCR genes by infiltrating
T-cells may indicate that a specific antigen in heart with myocarditis is
targeted. Our findings raise the possibility of immunotherapy with
monoclonal antibodies specific for TCR V beta elements to prevent
T-cell-mediated myocardial damage in viral myocarditis.
ARTICLES
T-cell receptor V beta gene expression in infiltrating cells in murine hearts with acute myocarditis caused by coxsackievirus B3
Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
This article has been cited by other articles:
![]() |
C. Kawai From Myocarditis to Cardiomyopathy: Mechanisms of Inflammation and Cell Death : Learning From the Past for the Future Circulation, March 2, 1999; 99(8): 1091 - 1100. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Seko, N. Takahashi, M. Azuma, H. Yagita, K. Okumura, and Y. Yazaki Expression of Costimulatory Molecule CD40 in Murine Heart With Acute Myocarditis and Reduction of Inflammation by Treatment With Anti-CD40L/B7-1 Monoclonal Antibodies Circ. Res., August 24, 1998; 83(4): 463 - 469. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Hanawa, T. Inomata, Y. Okura, S. Hirono, Y. Ogawa, T. Izumi, M. Kodama, and Y. Aizawa T Cells With Similar T-Cell Receptor ß-Chain Complementarity-Determining Region 3 Motifs Infiltrate Inflammatory Lesions of Synthetic Peptides Inducing Rat Autoimmune Myocarditis Circ. Res., July 27, 1998; 83(2): 133 - 140. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Seko, N. Takahashi, M. Azuma, H. Yagita, K. Okumura, and Y. Yazaki Effects of In Vivo Administration of Anti–B7-1/B7-2 Monoclonal Antibodies on Murine Acute Myocarditis Caused by Coxsackievirus B3 Circ. Res., March 23, 1998; 82(5): 613 - 618. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Hanawa, T. Inomata, H. Sekikawa, T. Abo, M. Kodama, T. Izumi, and A. Shibata Analysis of Heart-Infiltrating T-Cell Clonotypes in Experimental Autoimmune Myocarditis in Rats Circ. Res., January 1, 1996; 78(1): 118 - 125. [Abstract] [Full Text] |
||||
![]() |
H. Takada, C. Kishimoto, and Y. Hiraoka Therapy With Immunoglobulin Suppresses Myocarditis in a Murine Coxsackievirus B3 Model : Antiviral and Anti-inflammatory Effects Circulation, September 15, 1995; 92(6): 1604 - 1611. [Abstract] [Full Text] |
||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1994 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |