B型肝疾患における肝細胞障害機構の検討

片山 和宏; 林 紀夫; 竹原 徹郎; 砥綿 崇博; 結城 暢一; 春名 能通; 萩原 秀紀; 佐々木 裕; 笠原 彰紀; 房本 英之; 佐藤 信紘; 鎌田 武信

doi:10.2957/kanzo.31.1139

Study on the mechanism of liver cell injury in type B hepatitis

Kazuhiro KATAYAMA, Norio HAYASHI, Tetsuro TAKEHARA, Takahiro TOWATA, Nobukazu YUKI, Yoshimichi HARUNA, Hideki HAGIWARA, Yutaka SASAKI, Akinori KASAHARA, Hideyuki FUSAMOTO, Nobuhiro SATO, Takenobu KAMADA

Author information

Kazuhiro KATAYAMA
The First Department of Internal Medicine, Osaka University School of Medicine
Norio HAYASHI
The First Department of Internal Medicine, Osaka University School of Medicine
Tetsuro TAKEHARA
The First Department of Internal Medicine, Osaka University School of Medicine
Takahiro TOWATA
The First Department of Internal Medicine, Osaka University School of Medicine
Nobukazu YUKI
The First Department of Internal Medicine, Osaka University School of Medicine
Yoshimichi HARUNA
The First Department of Internal Medicine, Osaka University School of Medicine
Hideki HAGIWARA
The First Department of Internal Medicine, Osaka University School of Medicine
Yutaka SASAKI
The First Department of Internal Medicine, Osaka University School of Medicine
Akinori KASAHARA
The First Department of Internal Medicine, Osaka University School of Medicine
Hideyuki FUSAMOTO
The First Department of Internal Medicine, Osaka University School of Medicine
Nobuhiro SATO
The First Department of Internal Medicine, Osaka University School of Medicine
Takenobu KAMADA
The First Department of Internal Medicine, Osaka University School of Medicine

Keywords: α-interferon

JOURNAL FREE ACCESS

1990 Volume 31 Issue 10 Pages 1139-1142

DOI https://doi.org/10.2957/kanzo.31.1139

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Abstract

We studied the relationship between the expression of HLA class I antigen on hepatocytes and liver cell damage (hepatitis). The serum levels of GPT of patients positive for HLA class I antigen were significantly higher (p<0.01) than those of patients negative for it. Furthermore, the γ-IFN production of PHA-stimulated PBMCs from patients with active liver disease was enhanced in response to α-IFN. The responsiveness of PBMCs in response to α-IFN may be a cause of liver cell damage, by enhancing the expression of HLA class I Ag.

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