Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form
As of April 1st VIVO Scientific Profiles will no longer updated for faculty, and the link to VIVO will be removed from the library website. Faculty profile pages will continue to be updated via Interfolio. VIVO will continue being used behind the scenes to update graduate student profiles. Please contact helplib@scripps.edu if you have questions.
How to download citations from VIVO | Alternative profile options

Differential target cell sensitivity to CTL-activated death pathways in hepatitis B virus transgenic mice

Academic Article
uri icon
  • Overview
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Nakamoto, Y.
  • Guidotti, Luca
  • Pasquetto, V.
  • Schreiber, R. D.
  • Chisari, Francis

publication date

  • June 1997

journal

  • Journal of Immunology  Journal

abstract

  • The current study was designed to explore the relative contribution of Fas ligand (FasL), perforin, IFN-gamma, and TNF-alpha-induced death pathways in the pathogenesis of CTL-induced liver disease. Hepatitis B virus-specific CTL that are genetically unable to produce either FasL, perforin, or IFN-gamma were injected into Fas-competent and Fas-deficient hepatitis B virus transgenic mice that are either sensitive or resistant to the cytopathic effects of IFN-gamma based on the extent to which their hepatocytes retain hepatitis B surface Ag (HBsAg). The results of these experiments indicate that FasL- and perforin-dependent signals are primarily responsible for the induction of liver disease in the absence of HBsAg retention, but both signaling pathways must be activated simultaneously by the CTL in order to kill the hepatocyte in vivo. In contrast, neither FasL nor perforin are required to kill hepatocytes that retain HBsAg as long as the CTL secrete IFN-gamma on antigen recognition. Finally the results indicate that, irrespective of their HBsAg content, hepatocytes are much less sensitive to destruction by TNF-alpha than by the other death pathways. While all of these death pathways appear to be operative during a normal CTL response, the current experiments suggest that the target cell determines which pathway is dominant and selects its mode of execution.

subject areas

  • Animals
  • Antigens, Surface
  • Cell Death
  • Fas Ligand Protein
  • Hepatitis B Antigens
  • In Vitro Techniques
  • Interferon-gamma
  • Liver
  • Liver Diseases
  • Membrane Glycoproteins
  • Mice
  • Mice, Transgenic
  • Perforin
  • Pore Forming Cytotoxic Proteins
  • Signal Transduction
  • T-Lymphocytes, Cytotoxic
  • Tumor Necrosis Factor-alpha
scroll to property group menus

Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 9190918
scroll to property group menus

Additional Document Info

start page

  • 5692

end page

  • 5697

volume

  • 158

issue

  • 12

©2022 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support