Journal
JOURNAL OF IMMUNOLOGY
Volume 181, Issue 1, Pages 22-26Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.181.1.22
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Funding
- NIAID NIH HHS [AI040176, R56 AI040176, R01 AI040176, R01 AI040176-11] Funding Source: Medline
- NIGMS NIH HHS [R01 GM066182, R01 GM066182-04, GM066182] Funding Source: Medline
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Induced secretion of acute-phase serum amyloid A (SAA) is a host response to danger signals and a clinical indication of inflammation. The biological functions of SAA in inflammation have not been fully defined, although recent reports indicate that SAA induces proinflammatory cytokine expression. We now show that TLR2 is a functional receptor for SAA. HeLa cells expressing TLR2 responded to SAA with potent activation of NF-kappa B, which was enhanced by TLR1 expression and blocked by the Toll/IL-1 receptor/resistance (TIR) deletion mutants of TLR1, TLR2, and TLR6. SAA stimulation led to increased phosphorylation of MAPKs and accelerated I kappa B alpha degradation in TLR2-HeLa cells, and results from a solid-phase binding assay showed SAA interaction with the ectodomain of TLR2. Selective reduction of SAA-induced gene expression was observed in tlr2(-/-) mouse macrophages compared with wild-type cells. These results suggest a potential role for SAA in inflammatory diseases through activation of TLR2.
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