GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.
PMID:23082204
| Citation |
Soberman, RJ, MacKay, CR, Vaine, CA, Ryan, GB, Cerny, AM, Thompson, MR, Nikolic, B, Primo, V, Christmas, P, Sheiffele, P, Aronov, L, Knipe, DM and Kurt-Jones, EA (2012) CD200R1 supports HSV-1 viral replication and licenses pro-inflammatory signaling functions of TLR2. PLoS ONE 7:e47740 |
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| Abstract |
The CD200R1:CD200 axis is traditionally considered to limit tissue inflammation by down-regulating pro-inflammatory signaling in myeloid cells bearing the receptor. We generated CD200R1(-/-) mice and employed them to explore both the role of CD200R1 in regulating macrophage signaling via TLR2 as well as the host response to an in vivo, TLR2-dependent model, herpes simplex virus 1 (HSV-1) infection. CD200R1(-/-) peritoneal macrophages demonstrated a 70-75% decrease in the generation of IL-6 and CCL5 (Rantes) in response to the TLR2 agonist Pam(2)CSK(4) and to HSV-1. CD200R1(-/-) macrophages could neither up-regulate the expression of TLR2, nor assemble a functional inflammasome in response to HSV-1. CD200R1(-/-) mice were protected from HSV-1 infection and exhibited dysfunctional TLR2 signaling. Finally, both CD200R1(-/-) mice and CD200R1(-/-) fibroblasts and macrophages showed a markedly reduced ability to support HSV-1 replication. In summary, our data demonstrate an unanticipated and novel requirement for CD200R1 in "licensing" pro-inflammatory functions of TLR2 and in limiting viral replication that are supported by ex vivo and in vivo evidence. |
| Links |
PubMed PMC3474780 Online version:10.1371/journal.pone.0047740 |
| Keywords |
Animals; Antigens, Surface/metabolism; Brain/immunology; Brain/pathology; Brain/virology; Embryo, Mammalian/cytology; Encephalitis/immunology; Encephalitis/pathology; Encephalitis/virology; Fibroblasts/metabolism; Fibroblasts/pathology; Fibroblasts/virology; Gene Targeting; Herpesvirus 1, Human/physiology; Inflammation/immunology; Inflammation/pathology; Interferon Type I/biosynthesis; Macrophages, Peritoneal/immunology; Macrophages, Peritoneal/pathology; Macrophages, Peritoneal/virology; Mice; Receptors, Cell Surface/deficiency; Receptors, Cell Surface/metabolism; Signal Transduction/immunology; Toll-Like Receptor 2/metabolism; Viral Load/immunology; Virus Replication/physiology |
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