Circulation Research, Vol 67, 360-367, Copyright © 1990 by American Heart Association

ARTICLES

Expression of major histocompatibility complex class I antigen in murine ventricular myocytes infected with Coxsackievirus B3

Y Seko, H Tsuchimochi, T Nakamura, K Okumura, S Naito, K Imataka, J Fujii, F Takaku and Y Yazaki
Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan.

Evidence has accumulated that T cell-mediated autoimmunity plays an important role in the pathogenesis of viral myocarditis. T lymphocytes are known to recognize antigen-presenting cells, such as virus-infected cells, being restricted by syngeneic major histocompatibility complex (MHC) antigens. To clarify in more detail the immunological mechanisms involved, we induced acute viral myocarditis in C3H/He mouse ventricles with coxsackievirus B3 (CVB3) and examined, by immunofluorescence, the expression of MHC class I and II antigens, previously reported not to be expressed by normal cardiac myocytes. Furthermore, to confirm the expression of MHC class I (H-2Kk) antigens at the cellular level, we treated cultured cardiac myocytes with interferon gamma and examined the antigen expression by immunofluorescence and Northern blot hybridization, using an antisense RNA probe for MHC messenger RNA. Our observations demonstrated 1) CVB3-induced myocarditis resulted in the enhanced expression of MHC class I (H-2Kk) gene product on the surface of cardiac myocytes but low or undetectable levels of MHC class II or H- 2Dk gene products, and moderate focal transient (days 5-7) expression of both MHC class I (Kk + Dk) region gene products and MHC class II antigens were induced on capillary endothelial cells; 2) murine fetal cardiac myocytes cultured in vitro in the presence of interferon gamma similarly were shown to express marked levels of MHC class I (H-2Kk) but low to undetectable levels of the H-2Dk gene product; however, weak to moderate MHC Class II antigens were expressed by these cultured myocytes; and 3) the expression of MHC antigens in cardiac myocytes was modulated at the transcriptional level.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				J. W. Magnani and G. W. Dec Myocarditis: Current Trends in Diagnosis and Treatment Circulation, February 14, 2006; 113(6): 876 - 890. [Full Text] [PDF]

				Y. Seko, N. Kayagaki, K.-i. Seino, H. Yagita, K. Okumura, and R. Nagai Role of Fas/FasL pathway in the activation of infiltrating cells in murine acute myocarditis caused by Coxsackievirus B3 J. Am. Coll. Cardiol., April 17, 2002; 39(8): 1399 - 1403. [Abstract] [Full Text] [PDF]

				A. M. Feldman and D. McNamara Myocarditis N. Engl. J. Med., November 9, 2000; 343(19): 1388 - 1398. [Full Text] [PDF]

				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]

				J. R. Gebhard, C. M. Perry, S. Harkins, T. Lane, I. Mena, V. C. Asensio, I. L. Campbell, and J. L. Whitton Coxsackievirus B3-Induced Myocarditis : Perforin Exacerbates Disease, But Plays No Detectable Role in Virus Clearance Am. J. Pathol., August 1, 1998; 153(2): 417 - 428. [Abstract] [Full Text] [PDF]