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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Membrane-anchored CD14 is required for LPS- induced TLR4 endocytosis in TLR4/MD-2/CD14 overexpressing CHO cells.

Lipopolysaccharide (LPS) induces inflammatory activation through TLR4 (toll-like receptor-4)/MD-2 (myeloid differentiation-2)/CD14 (cluster of differentiation-14) complex. Although optimal LPS signaling is required to activate our innate immune systems against gram-negative bacterium, excessive amount of LPS signaling develops a detrimental inflammatory response in gram-negative bacterial infections. Downregulation of surface TLR4 expression is one of the critical mechanisms that can restrict LPS signaling. Here, we found that membrane-anchored CD14 is required for LPS- induced downregulation of TLR4 and MD-2 in CHO cells. Moreover, pretreatment of the cells with sterol-binding agent filipin reduced LPS-induced TLR4 downregulation, suggesting the involvement of caveolae-mediated endocytosis pathway. Involvement of caveolae in LPS-induced TLR4 endocytosis was further confirmed by immunoprecipitation. Thus, our data indicate that caveolae-dependent endocytosis pathway is involved in LPS-induced TLR4 downregulation and that this is dependent on membrane-anchored CD14 expression.[1]

References

  1. Membrane-anchored CD14 is required for LPS-induced TLR4 endocytosis in TLR4/MD-2/CD14 overexpressing CHO cells. Shuto, T., Kato, K., Mori, Y., Viriyakosol, S., Oba, M., Furuta, T., Okiyoneda, T., Arima, H., Suico, M.A., Kai, H. Biochem. Biophys. Res. Commun. (2005) [Pubmed]
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