Human dendritic cells that lack IRAK-4 (gray bars) do not produce inflammatory cytokines in response to most TLR signals.
The TLRs are part of an early infection warning system that recognizes microbial intrusion. Many activated TLRs recruit a kinase called IRAK-4, which switches on immune-boosting transcription pathways.
In mice, IRAK-4 is thought to be a crucial cog in innate defense, as mice of all ages lacking the kinase are vulnerable to many different viruses, bacteria, and fungi. But the human version now appears to be less comprehensive.
The new study examined 28 patients with IRAK-4 mutations. Immune cells from these patients' blood failed to produce inflammatory cytokines in response to TLR...
The Rockefeller University Press
2007
The Rockefeller University Press
2007
You do not currently have access to this content.