Increased severity of viral myocarditis in mice lacking lymphocyte maturation. (Q54102735)

24 May 2018

title

Increased severity of viral myocarditis in mice lacking lymphocyte maturation. (English)

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24 May 2018

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Kanda T

1

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Koike H

2

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Arai M

3

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Wilson JE

4

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Carthy CM

5

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Yang D

6

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McManus BM

7

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Nagai R

8

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Kobayashi I

9

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language of work or name

English

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publication date

1 January 1999

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24 May 2018

International Journal of Cardiology

published in

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volume

68

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issue

1

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page(s)

13-22

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Mechanisms of immune-mediated myocyte injury

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In vivo significance of T cells in the development of Coxsackievirus B3 myocarditis in mice. Immature but antigen-specific T cells aggravate cardiac injury

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Cytotoxic and viral neutralizing antibodies crossreact with streptococcal M protein, enteroviruses, and human cardiac myosin

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RAG-2-deficient mice lack mature lymphocytes owing to inability to initiate V(D)J rearrangement

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Cell death mechanisms and the immune system

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Potential roles of apoptosis in viral pathogenesis

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Tumor necrosis factor alpha-induced apoptosis in cardiac myocytes. Involvement of the sphingolipid signaling cascade in cardiac cell death

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The comet assay: a comprehensive review

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Hypoxia induces apoptosis with enhanced expression of Fas antigen messenger RNA in cultured neonatal rat cardiomyocytes

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Reperfusion injury induces apoptosis in rabbit cardiomyocytes

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Apoptosis in pressure overload-induced heart hypertrophy in the rat.

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Modification of viral myocarditis in mice by interleukin-6

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Apoptosis by death factor

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New Paradigm for Lymphocyte Granule-mediated Cytotoxicity

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Regulation of apoptosis by viral gene products

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Direct interactions of coxsackievirus B3 with immune cells in the splenic compartment of mice susceptible or resistant to myocarditis

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7 January 2021

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Identifiers

DOI

1 reference

24 May 2018

PubMed ID

10077396

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24 May 2018