Journal
BLOOD
Volume 103, Issue 4, Pages 1433-1437Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2003-08-2674
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Funding
- NCI NIH HHS [CA94056] Funding Source: Medline
- NEI NIH HHS [R01 EY009083, R01 EY09083] Funding Source: Medline
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Natural interferon-producing cells (IPCs) specialize in the production of high levels of type 1 interferons (IFNs) in response to encapsulated DNA and RNA viruses. Here we demonstrate that the secretion of type 1 IFN in response to herpes simplex virus type 1 (HSV-1) in vitro is mediated by the toll-like receptor 9 (TLR9)/MyD88 pathway. Moreover, IPCs produce interleukin-12 (IL-12) in response to HSV-1 in vitro, which is also dependent on TLR9/ MyD88 signaling. Remarkably, though TLR9/MyD88-deficiency abrogates IPC responses to HSV-1 in vitro, mice lacking either MyD88 or TLR9 are capable of controlling HSV-1 replication in vivo after local infection, demonstrating that TLR9 and MyD88-Independent pathways in cells other than IPCs can effectively compensate for defective IPC responses to HSV-1.
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