Neurons induced to express major histocompatibility complex class I antigen are killed via the perforin and not the Fas (APO-1/CD95) pathway
Details
Serval ID
serval:BIB_1288B570CADD
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Neurons induced to express major histocompatibility complex class I antigen are killed via the perforin and not the Fas (APO-1/CD95) pathway
Journal
European Journal of Immunology
ISSN
0014-2980 (Print)
Publication state
Published
Issued date
09/1996
Volume
26
Number
9
Pages
2271-4
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Sep
Research Support, Non-U.S. Gov't --- Old month value: Sep
Abstract
Cytotoxic T lymphocytes (CTL) kill target cells by perforin-mediated pore formation, induction of apoptosis by the Fas ligand, or both. It has been demonstrated that depolarized neurons can be induced to express major histocompatibility complex (MHC) class I antigens by interferon-gamma. Evidence for antigen-dependent CTL-mediated killing was obtained by transfecting neurons with MHC class I cDNA. The present study was designed to investigate the mechanisms of killing of cerebellar granule neurons depolarized by high K+ concentrations and thereby inducible for MHC class I antigen expression. We found that neurons express only low levels of Fas (APO-1/CD95) and are resistant to Fas ligand-mediated killing even when pretreated with cytokines. However, granules extracted from CTL as well as purified perforin induce almost complete lysis of neurons. These data suggest that CTL-mediated elimination of neurons involves the perforin, but not the Fas pathway of target cell killing.
Keywords
Animals
Antigens, CD95/*physiology
Cytotoxicity, Immunologic
Histocompatibility Antigens Class I/*physiology
Interferon Type II/pharmacology
Interferon-alpha/pharmacology
Membrane Glycoproteins/*physiology
Mice
Mice, Inbred C57BL
Neurons/*immunology
Pore Forming Cytotoxic Proteins
T-Lymphocytes, Cytotoxic/*physiology
Pubmed
Web of science
Create date
24/01/2008 15:19
Last modification date
20/08/2019 12:40