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Tetsuya Ishikawa

Researcher at Nagoya University

Publications -  203
Citations -  7094

Tetsuya Ishikawa is an academic researcher from Nagoya University. The author has contributed to research in topics: Hepatitis B virus & Hepatitis. The author has an hindex of 38, co-authored 185 publications receiving 6669 citations. Previous affiliations of Tetsuya Ishikawa include RMIT University & Scripps Research Institute.

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Intracellular inactivation of the hepatitis B virus by cytotoxic T lymphocytes

TL;DR: A transgenic mouse model of HBV replication is used to demonstrate that adoptively transferred virus-specific CTLs can abolish HBV gene expression and replication in the liver without killing the hepatocytes.
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Detection of hepatitis C virus by polymerase chain reaction and response to interferon-α therapy: Relationship to genotypes of hepatitis C virus

TL;DR: Results indicate that detection of hepatitis C virus RNA by polymerase chain reactions with different sets of primers and probes may be valuable in classifying hepatitis Cirus into genotypes, and that amount of hepatitisC virus RNA in sera and response to interferon‐α may vary among different genotypes of HCV.
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Cytotoxic T lymphocytes inhibit hepatitis B virus gene expression by a noncytolytic mechanism in transgenic mice

TL;DR: It is demonstrated that class I-restricted HBV-specific CTLs profoundly suppress hepatocellular HBV gene expression in HBV transgenic mice by a noncytolytic process, the strength of which greatly exceeds the cytopathic effect of the C TLs in magnitude and duration.
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Class I-restricted cytotoxic T lymphocytes are directly cytopathic for their target cells in vivo.

TL;DR: It is demonstrated that CD8-positive, Ld-restricted hepatitis B surface Ag-specific CTL bind and kill their target cells in vivo by triggering them to undergo degenerative cytologic changes compatible with apoptosis.
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Serum levels of IL-10, IL-15 and soluble tumour necrosis factor-alpha (TNF-α) receptors in type C chronic liver disease

TL;DR: Serum levels of these molecules correlated with disease progress in chronic HCV infection, and that IL‐10 and IL‐15 may reflect the degree of inflammation in the liver, indicate that both cytokines may be related to the development of HCC.