Journal
IMMUNITY
Volume 17, Issue 3, Pages 251-263Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(02)00390-4
Keywords
-
Categories
Funding
- NCI NIH HHS [5-T32-CA009120-26, R01 CA87924] Funding Source: Medline
- NIAID NIH HHS [R37 AI47868] Funding Source: Medline
- NIGMS NIH HHS [R01 GM57559, GM 08042] Funding Source: Medline
Ask authors/readers for more resources
We have identified a subset of genes that is specifically induced by stimulation of TLR3 or TLR4 but not by TLR2 or TLR9. Further gene expression analyses established that upregulation of several primary response genes was dependent on NF-kappaB, commonly activated by several TLRs, and interferon regulatory factor 3 (IRF3), which was found to confer TLR3/TLR4 specificity. Also identified was a group of secondary response genes which are part of an autocrine/paracrine loop activated by the primary response gene product, interferon beta (IFNbeta). Selective activation of the TLR3/TLR4-IRF3 pathway potently inhibited viral replication. These results suggest that TLR3 and TLR4 have evolutionarily diverged from other TLRs to activate IRF3, which mediates a specific gene program responsible for innate antiviral responses.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available