Cutting Edge: Endotoxin Tolerance in Mouse Peritoneal Macrophages Correlates with Down-Regulation of Surface Toll-Like Receptor 4 Expression1
By Fumiko Nomura, S. Akashi, Yoshimitsu Sakao, Shintaro Sato, Taro Kawai, M. Matsumoto, K. Nakanishi, M. Kimoto, K. Miyake, K. Takeda and 1 more. Journal of Immunology, 2000
862 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology
View Paper: https://www.semanticscholar.org/paper/3c0f255d4b17685b4cfcf179c38fe6d1e5cb075e
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Citations in the corpus
- Akt1 controls macrophage response to LPS by regulating microRNAs (2009, methodology): “Thus, within a few hours from the start of LPS stimulation, the expression of the LPS receptor TLR4 decreases, to rise again 24 to 48 hr later (Medvedev et al., 2000; Nomura et al., 2000).”
- Oligosaccharides of Hyaluronan Activate Dendritic Cells via Toll-like Receptor 4 (2002, background): “Moreover, ligation of the TLR-4 complex by LPS in mouse macrophages occurs very rapidly, with the receptor being downregulated within 1 h after stimulation (40).”
- Differential Alteration in Intestinal Epithelial Cell Expression of Toll-Like Receptor 3 (TLR3) and TLR4 in Inflammatory Bowel Disease (2000, background): “This tolerance could result from TLR4 downregulation minimizing LPS recognition, given that primary IECs in normal tissue appear to express very little, if any, TLR4 (28).”
- Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock (2003, background): “Although LPS induces an increase in TLR4 mRNA in a number of cell types, surface expression of TLR4 is decreased on murine macrophages (348, 390) and human monocytes (47).”