Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form

Viral persistence in neurons explained by lack of major histocompatibility class-1 expression

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

Overview

authors

  • Joly, E.
  • Mucke, L.
  • Oldstone, Michael

publication date

  • September 1991

journal

  • Science  Journal

abstract

  • Viruses frequently persist in neurons, suggesting that these cells can evade immune surveillance. In a mouse model, 5 x 10(6) cytotoxic T lymphocytes (CTLs), specific for lymphocytic choriomeningitis virus (LCMV), did not lyse infected neurons or cause immunopathologic injury. In contrast, intracerebral injection of less than 10(3) CTL caused disease and death when viral antigens were expressed on leptomeningeal and choroid plexus cells of the nervous system. The neuronal cell line OBL21 expresses little or no major histocompatibility (MHC) class I surface glycoproteins and when infected with LCMV, resisted lysis by virus-specific CTLs. Expression of MHC heavy chain messenger RNA was limited, but beta 2-microglobulin messenger RNA and protein was made normally. OBL21 cells were made sensitive to CTL lysis by transfection with a fusion gene encoding another MHC class I molecule. Hence, neuronal cells probably evade immune surveillance by failing to express MHC class I molecules.

subject areas

  • Acute Disease
  • Animals
  • Brain
  • Cell Line
  • Chronic Disease
  • Gene Expression
  • Genes, MHC Class I
  • Histocompatibility Antigens Class I
  • Lymphocytic Choriomeningitis
  • Lymphocytic choriomeningitis virus
  • Mice
  • Mice, Inbred Strains
  • Neurons
  • T-Lymphocytes, Cytotoxic
scroll to property group menus

Identity

International Standard Serial Number (ISSN)

  • 0036-8075

Digital Object Identifier (DOI)

  • 10.1126/science.1891717

PubMed ID

  • 1891717
scroll to property group menus

Additional Document Info

start page

  • 1283

end page

  • 1285

volume

  • 253

issue

  • 5025

©2021 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support