Role of Fas/FasL pathway in the activation of infiltrating cells in murine acute myocarditis caused by Coxsackievirus B3
Yoshinori Seko, MD*  ,*,
Nobuhiko Kayagaki, PhD,
Ken-ichiro Seino, MD,
Hideo Yagita, PhD,
Ko Okumura, PhD and
Ryozo Nagai, MD*
* Department of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
Department of Immunology, School of Medicine, Juntendo University, Tokyo, Japan
Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan
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Figure 1 Immunohistochemical study for Fas in ventricular tissue. Normal ventricular myocardium (A) and ventricular myocardium of mice on day 7 (B), at two weeks (C to E) and at six weeks (F) after Coxsackie virus B3 infection were stained with anti-Fas antibody. Bar = 20 µm.
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Figure 2 Immunocytochemical study of cultured cardiac myocytes for Fas. (A and B) Myocytes in control group (A) and interferon-gamma-treated group (B), stained with anti-Fas antibody and labeled with fluorescein isothiocyanate. (C and D) Myocytes stained with a mAb for cardiac myosin heavy chain (CMA19) and labeled with tetramethylrhodamine isothiocyanate, corresponding to A and B, respectively. Bar = 10 µm.
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Figure 3 Effects of anti-FasL monoclonal antibody (mAb) treatment on the expression of proinflammatory cytokine transcripts and Coxsackie virus B3 (CVB3) genomes in the ventricular tissues. Total ribonucleic acid was prepared from ventricular tissues of mice from mouse immunoglobulin G (IgG)-treated control group and anti-FasL mAb-treated group, and analyzed for CVB3, interferon (IFN)-gamma, interleukin (IL)-2, inducible nitric oxide synthase (iNOS) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) transcripts by a semiquantitative polymerase chain reaction method.
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