PMID- 12797446
OWN - NLM
STAT- MEDLINE
DCOM- 20030630
LR  - 20211203
IS  - 0070-217X (Print)
IS  - 2196-9965 (Electronic)
IS  - 0070-217X (Linking)
VI  - 276
DP  - 2003
TI  - Infection of dendritic cells by lymphocytic choriomeningitis virus.
PG  - 125-44
AB  - Dendritic cells (DCs) comprise the major antigen-presenting cells (APCs) of the 
      host, uniquely programmed to stimulate immunologically naive 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.
FAU - Sevilla, N
AU  - Sevilla N
AD  - The Scripps Research Institute, Division of Virology, Department of 
      Neuropharmacology, 10550 N. Torrey Pines Road, La Jolla, CA 92037, USA.
FAU - Kunz, S
AU  - Kunz S
FAU - McGavern, D
AU  - McGavern D
FAU - Oldstone, M B A
AU  - Oldstone MB
LA  - eng
GR  - R21 NS048866/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - Germany
TA  - Curr Top Microbiol Immunol
JT  - Current topics in microbiology and immunology
JID - 0110513
RN  - 0 (Cytoskeletal Proteins)
RN  - 0 (DAG1 protein, human)
RN  - 0 (Membrane Glycoproteins)
RN  - 146888-27-9 (Dystroglycans)
SB  - IM
MH  - Animals
MH  - Cytoskeletal Proteins/*metabolism
MH  - Dendritic Cells/immunology/metabolism/pathology/*virology
MH  - Dystroglycans
MH  - Humans
MH  - Immunosuppression Therapy
MH  - Lymphocytic choriomeningitis virus/isolation & 
      purification/*metabolism/pathogenicity/physiology
MH  - Membrane Glycoproteins/*metabolism
MH  - Spleen/metabolism/virology
MH  - Virus Replication
PMC - PMC5321679
MID - NIHMS849859
EDAT- 2003/06/12 05:00
MHDA- 2003/07/02 05:00
PMCR- 2017/02/23
CRDT- 2003/06/12 05:00
PHST- 2003/06/12 05:00 [pubmed]
PHST- 2003/07/02 05:00 [medline]
PHST- 2003/06/12 05:00 [entrez]
PHST- 2017/02/23 00:00 [pmc-release]
AID - 10.1007/978-3-662-06508-2_6 [doi]
PST - ppublish
SO  - Curr Top Microbiol Immunol. 2003;276:125-44. doi: 10.1007/978-3-662-06508-2_6.