Cutting Edge: TLR2-Deficient and MyD88-Deficient Mice Are Highly Susceptible to Staphylococcus aureus Infection1

By O. Takeuchi, K. Hoshino, Shizuo Akira. Journal of Immunology, 2000

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The Role of TLR2 in Infection and Immunity (2012, background): “…antibodies or gene knockouts, when exposed to the above bacteria or their cell wall components have diminished or absent production of TNF-α or/and IL-6, as opposed to normal cells (Takeuchi et al., 1999, 2000; Torres et al., 2004; Bafica et al., 2005; Leendertse et al., 2008; Love et al., 2010).”
Human Cytomegalovirus Activates Inflammatory Cytokine Responses via CD14 and Toll-Like Receptor 2 (2003, methodology): “TLR2-deficient mice were engineered as described previously (55) and were the”
Toll-like receptors and their crosstalk with other innate receptors in infection and immunity. (2011, background): “MyD88-deficient mice are more susceptible to infection than TLR2-deficient mice in various infection models (Miller et al., 2006; Takeuchi et al., 2000), suggesting a contribution by other TLRs and/or members of IL-1 receptor family.”
NF-κB and the immune response (2006, background): “TLR2 also mediates responses to several Gram-positive bacterial cell wall components as well as Staphylococcus aureus peptidoglycan (Takeuchi et al., 2000).”
Tissue Expression of Human Toll-Like Receptors and Differential Regulation of Toll-Like Receptor mRNAs in Leukocytes in Response to Microbes, Their Products, and Cytokines (2002, background): “ceptible (10) and demonstrate the role of TLR2 in responses to”