SIGIRR, a negative regulator of Toll-like receptor–interleukin 1 receptor signaling
Copyright policy )SIGIRR, a negative regulator of Toll-like receptor–interleukin 1 receptor signaling
The Toll-like receptor-interleukin 1 receptor signaling (TLR-IL-1R) receptor superfamily is important in differentially recognizing pathogen products and eliciting appropriate immune responses. These receptors alter gene expression, mainly through the activation of nuclear factor-kappaB and activating protein 1. SIGIRR (single immunoglobulin IL-1R-related molecule), a member of this family that does not activate these factors, instead negatively modulates immune responses. Inflammation is enhanced in SIGIRR-deficient mice, as shown by their enhanced chemokine induction after IL-1 injection and reduced threshold for lethal endotoxin challenge. Cells from SIGIRR-deficient mice showed enhanced activation in response to either IL-1 or certain Toll ligands. Finally, biochemical analysis indicated that SIGIRR binds to the TLR-IL-1R signaling components in a ligand-dependent way. Our data show that SIGIRR functions as a biologically important modulator of TLR-IL-1R signaling.
- Cleveland Clinic United States
- Amgen (United States) United States
Lipopolysaccharides, Mice, Knockout, Mice, Inbred BALB C, Membrane Glycoproteins, Immunoblotting, Toll-Like Receptors, Interleukin-18, NF-kappa B, Receptors, Interleukin-1, Receptors, Cell Surface, Mice, Inbred C57BL, Jurkat Cells, Mice, Gene Expression Regulation, Animals, Humans, RNA, Chemokines, Interleukin-1, Signal Transduction
Lipopolysaccharides, Mice, Knockout, Mice, Inbred BALB C, Membrane Glycoproteins, Immunoblotting, Toll-Like Receptors, Interleukin-18, NF-kappa B, Receptors, Interleukin-1, Receptors, Cell Surface, Mice, Inbred C57BL, Jurkat Cells, Mice, Gene Expression Regulation, Animals, Humans, RNA, Chemokines, Interleukin-1, Signal Transduction
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