Article: article from journal or magazin.
Immunosuppression and resultant viral persistence by specific viral targeting of dendritic cells.
Journal of Experimental Medicine
Among cells of the immune system, CD11c(+) and DEC-205(+) splenic dendritic cells primarily express the cellular receptor (alpha-dystroglycan [alpha-DG]) for lymphocytic choriomeningitis virus (LCMV). By selection, strains and variants of LCMV that bind alpha-DG with high affinity are associated with virus replication in the white pulp, show preferential replication in a majority of CD11c(+) and DEC-205(+) cells, cause immunosuppression, and establish a persistent infection. In contrast, viral strains and variants that bind with low affinity to alpha-DG are associated with viral replication in the red pulp, display minimal replication in CD11c(+) and DEC-205(+) cells, and generate a robust anti-LCMV cytotoxic T lymphocyte response that clears the virus infection. Differences in binding affinities can be mapped to a single amino acid change in the viral glycoprotein 1 ligand that binds to alpha-DG. These findings indicate that receptor-virus interaction on dendritic cells in vivo can be an essential step in the initiation of virus-induced immunosuppression and viral persistence.
Animals, Antigens, CD, Antigens, CD11/immunology, Cell Line, Central Nervous System/virology, Chronic Disease, Cricetinae, Cytoskeletal Proteins/metabolism, Dendritic Cells/immunology, Dendritic Cells/metabolism, Dystroglycans, Immunosuppression, In Situ Hybridization, Lectins, C-Type, Lymphocytic Choriomeningitis/immunology, Lymphocytic Choriomeningitis/virology, Lymphocytic choriomeningitis virus/genetics, Lymphocytic choriomeningitis virus/immunology, Membrane Glycoproteins/analysis, Membrane Glycoproteins/metabolism, Mice, Mice, Inbred BALB C, Mice, Knockout, Protein Binding, Receptors, Cell Surface/analysis, Receptors, Virus/metabolism, Spleen/cytology, Spleen/immunology, T-Lymphocytes, Cytotoxic/immunology, Tumor Necrosis Factor-alpha/genetics, Tumor Necrosis Factor-alpha/physiology, Viral Proteins/genetics, Viral Proteins/metabolism, Virus Replication
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