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Kazuki Ando

Researcher at Gifu University

Publications -  33
Citations -  2291

Kazuki Ando is an academic researcher from Gifu University. The author has contributed to research in topics: Hepatitis B virus & CTL*. The author has an hindex of 21, co-authored 33 publications receiving 2240 citations. Previous affiliations of Kazuki Ando include International Agency for Research on Cancer & Scripps Research Institute.

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Mechanisms of class I restricted immunopathology. A transgenic mouse model of fulminant hepatitis.

TL;DR: The principles illustrated in this study are generally applicable to other models of class I-restricted, CTL-induced immunopathology, and it is suggested that they contribute to the immunopathogenesis of viral hepatitis during hepatitis B virus infection in humans.
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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.
Journal Article

Perforin, Fas/Fas ligand, and TNF-alpha pathways as specific and bystander killing mechanisms of hepatitis C virus-specific human CTL.

TL;DR: It is shown that HCV-specific CTL clones kill non-Ag-bearing bystander cells as well as Ag-bearing cells, although the bystander killing is less efficient than the specific target cell killing, and the efficacy of the bystanderser killing of anti-Fas- and soluble TNF-alpha-sensitive cells is greater than that of resistant cells.
Journal Article

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.
Journal Article

CTL access to tissue antigen is restricted in vivo.

TL;DR: The results suggest that viral, tumor, and normal self Ags expressed in the liver are readily accessible to class I-restricted T cells, whereas the vascular endothelium and/or the vascular and cellular basement membranes constitute an extremely effective barrier that precludes CTL access to tissue Ag at many other sites.