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CD200 Receptor Restriction of Myeloid Cell Responses Antagonizes Antiviral Immunity and Facilitates Cytomegalovirus Persistence within Mucosal Tissue


Immune inhibitory receptors, including CD200 receptor (CD200R), can limit immune responses in the mucosa to restrict reactivity to the plethora of harmless antigens that mucosal surfaces are continually exposed to. However, viruses may exploit these suppressive mechanisms to enable their persistence and spread. Many viruses, including herpesviruses, have acquired functional homologs of CD200, the ligand of CD200R, implying that viral exploitation of this pathway is evolutionary advantageous. We now show that the β-herpesvirus murine cytomegalovirus (MCMV) takes advantage of the CD200R inhibitory pathway to persist within a mucosal site of MCMV persistence, the salivary glands. Mice deficient in CD200R mounted elevated antiviral immune responses that were driven by the increased division and accumulation of myeloid cells that function to orchestrate the generation of antiviral effector immune responses. Interestingly, MCMV infection of myeloid cells up-regulated CD200 expression. Thus, MCMV exploits the CD200 pathway to persist within mucosal tissue.


Vyšlo v časopise: CD200 Receptor Restriction of Myeloid Cell Responses Antagonizes Antiviral Immunity and Facilitates Cytomegalovirus Persistence within Mucosal Tissue. PLoS Pathog 11(2): e32767. doi:10.1371/journal.ppat.1004641
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004641

Souhrn

Immune inhibitory receptors, including CD200 receptor (CD200R), can limit immune responses in the mucosa to restrict reactivity to the plethora of harmless antigens that mucosal surfaces are continually exposed to. However, viruses may exploit these suppressive mechanisms to enable their persistence and spread. Many viruses, including herpesviruses, have acquired functional homologs of CD200, the ligand of CD200R, implying that viral exploitation of this pathway is evolutionary advantageous. We now show that the β-herpesvirus murine cytomegalovirus (MCMV) takes advantage of the CD200R inhibitory pathway to persist within a mucosal site of MCMV persistence, the salivary glands. Mice deficient in CD200R mounted elevated antiviral immune responses that were driven by the increased division and accumulation of myeloid cells that function to orchestrate the generation of antiviral effector immune responses. Interestingly, MCMV infection of myeloid cells up-regulated CD200 expression. Thus, MCMV exploits the CD200 pathway to persist within mucosal tissue.


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