Infection of dendritic cells by lymphocytic choriomeningitis virus.

Details

Serval ID
serval:BIB_11929F1DC852
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Title
Infection of dendritic cells by lymphocytic choriomeningitis virus.
Journal
Current Topics in Microbiology and Immunology
Author(s)
Sevilla N., Kunz S., McGavern D., Oldstone M.B.
ISSN
0070-217X (Print)
ISSN-L
0070-217X
Publication state
Published
Issued date
2003
Volume
276
Pages
125-144
Language
english
Abstract
Dendritic cells (DCs) comprise the major antigen-presenting cells (APCs) of the host, uniquely programmed to stimulate immunologically naïve T lymphocytes. Viruses that can target and disorder the function of these cells enjoy a selective advantage. The cellular receptor for lymphocytic choriomeningitis virus (LCMV), Lassa fever virus (LFV), and several other arenaviruses is alpha-dystroglycan (alpha-DG). Among cells of the immune system, CD11c+ and DEC-205+ DCs primarily and preferentially express alpha-DG. By selection, strains and variants of LCMV generated as quasi-species that bind alpha-DG with high affinity replicate in the majority of CD11c+ and DEC-205+ (>75%) DCs, causing a generalized immunosuppression, and establish a persistent infection. In contrast, viral strains and variants that bind with low affinity to alpha-DG display minimal replication in CD11c+ and DEC-205+ DCs (<10%), rarely replicate in the white pulp, and generate a robust anti-LCMV CTL response that clears the virus infection. Hence, receptor-virus interaction on DCs in vivo is an essential step in the initiation of virus-induced immunosuppression and viral persistence. Investigation into the mechanism of how virus-infected DCs cause immunosuppression reveals loss of MHC class II surface expression and costimulatory molecules on surface of such DCs. As a consequence DCs are unable to act as APCs, initiate immune responses, and have a defect in migration into the T cell area. These data indicate that LCMV infection influences DC maturation and migration, leading to decreased T cell stimulatory capacity of DCs, events essential for the initiation of immune responses. Because several other viruses known to cause immunosuppression (HIV, measles) interact with DCs, the observations noted here are likely a common selective mechanism by which viruses also are able to evade the host's immune system.
Keywords
Animals, Cytoskeletal Proteins/metabolism, Dendritic Cells/immunology, Dendritic Cells/metabolism, Dystroglycans, Humans, Immunosuppression, Lymphocytic choriomeningitis virus/isolation & purification, Lymphocytic choriomeningitis virus/metabolism, Membrane Glycoproteins/metabolism, Spleen/metabolism, Spleen/virology, Virus Replication
Pubmed
Web of science
Create date
17/04/2013 16:46
Last modification date
20/08/2019 12:39
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