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CD200R1 supports HSV-1 viral replication and licenses pro-inflammatory signaling functions of TLR2.

PloS one | Oct 19, 2012

http://www.ncbi.nlm.nih.gov/pubmed/23082204

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.

Pubmed ID: 23082204 RIS Download

Mesh terms: Animals | Antigens, Surface | Brain | Embryo, Mammalian | Encephalitis | Fibroblasts | Gene Targeting | Herpesvirus 1, Human | Inflammation | Interferon Type I | Macrophages, Peritoneal | Mice | Orexin Receptors | Receptors, Cell Surface | Signal Transduction | Toll-Like Receptor 2 | Viral Load | Virus Replication

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Associated grants

  • Agency: NIAID NIH HHS, Id: 5P30 AI-42845
  • Agency: NIDDK NIH HHS, Id: DK32520
  • Agency: NIAID NIH HHS, Id: P01 AI083215-01
  • Agency: NIAID NIH HHS, Id: R01AI068871
  • Agency: NIAID NIH HHS, Id: R01AI068871-S4
  • Agency: NIAID NIH HHS, Id: T32 AI095213

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