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

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


  • Soberman RJ
  • MacKay CR
  • Vaine CA
  • Ryan GB
  • Cerny AM
  • Thompson MR
  • Nikolic B
  • Primo V
  • Christmas P
  • Sheiffele P
  • Aronov L
  • Knipe DM
  • Kurt-Jones EA


PloS one

Publication Data

October 19, 2012

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

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