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AssigneeThe Board of Trustees of the University of Illinois
InventorsRichard D. Ye, Ni Cheng, Rong L. He
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The present disclosure relates to compositions and methods of modulating inflammatory and immune responses through binding of SAA to TLR2 in a subject (e.g., human, non-human primate, rodent, etc.), and compositions and methods for screening TLR2 agonists and antagonists. In the studies described herein, a potential role of SAA in neutrophilia was investigated and the results demonstrated that SAA is a potent inducer for macrophage secretion of G-CSF, which leads to neutrophilia in mice. Using G-CSF−/− and TLR2−/− mice, it was found that the SAA-induced neutrophilia is dependent on TLR2-mediated production of G-CSF. Based on direct binding assay and gain-of-function studies in TLR2-transfected cells, SAA was identified as a novel ligand for TLR2 and a link between increased SAA concentration and TLR2-mediated inflammatory responses such as neutrophilia was established. Additional embodiments are disclosed.
A method comprising providing a composition comprising SAA protein or a nucleic acid encoding SAA protein, and administering the composition to a subject,
A method comprising:
A method comprising:
A method comprising providing a composition comprising a TLR2 antagonist and contacting a plurality of cells with the composition,
A HeLa cell comprising a first purified nucleic acid encoding TLR2 and a second purified nucleic acid comprising a plurality of NF-κB binding sites operably linked to at least one expression control sequence and a reporter gene.
Dependencies are inferred from the claim text.