TLR4, but not TLR2, mediates IFN-β–induced STAT1α/β-dependent gene expression in macrophages

By Vladimir Toshchakov, Bryan W. Jones, P. Perera, K. Thomas, M. J. Cody, Shuling Zhang, B. Williams, J. Major, T. Hamilton, M. Fenton and 1 more. Nature Immunology, 2002

712 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/960fb89b76ef73c66d98a4bac37e652be94e97c8

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1. Brittney R. Coats
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Citations in the corpus

• Toll-like receptors. (2003, background): “Bacterial infection or LPS stimulation of macrophages leads to the rapid phosphorylation of a serine residue in Stat1 (253).”
• Metabolic dysfunction drives a mechanistically distinct proinflammatory phenotype in adipose tissue macrophages. (2014, background): “Moreover, this concept may not be restricted to settings of sterile inflammation, as bacterial products that are primarily recognized by TLR2 also produce inflammation without activating the type I interferon response (Toshchakov et al., 2002), an observation that we confirmed experimentally.”