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- W4313384997 abstract "Abstract TLR4 signaling is critical for providing effective immune protection but must be tightly controlled to avoid inflammation-induced pathology. Previously, we reported extensive and direct interactions between TLR and Siglec families of Pattern Recognition Receptors. Here, we examined the biological significance of this interaction during infection. We found that Siglec-E is required for E. coli-induced endocytosis of TLR4. Siglec-E-deficient dendritic cells infected with E. coli fail to internalize TLR4. This leads to sustained TLR4 on cell surface and activation of NF-κB and MAP kinase p38, resulting in high levels of TNF-α and IL-6 compared with wild-type dendritic cells. In contrast to the signaling events occurring at the plasma membrane, as a result of the inability to internalize of TLR4, Siglec-E-deficient dendritic cells were also defective for TRIF-mediated IFN-β production in response to E. coli infection. Furthermore, we found that accumulation of ubiquitinated-TLR4 and binding of E3 ubiquitin ligase Triad3A to TLR4 was increased significantly in bone marrow-derived dendritic cells from wild-type mice, but not from Siglec-E-deficient mice, after E. coli infection. This represents a newly discovered mechanism that regulates the signaling of TLR4 during E. coli infection." @default.
- W4313384997 created "2023-01-06" @default.
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- W4313384997 date "2017-05-01" @default.
- W4313384997 modified "2023-09-26" @default.
- W4313384997 title "Siglec-E negatively regulates the activation of Toll-like Receptor 4 by controlling its endocytosis" @default.
- W4313384997 doi "https://doi.org/10.4049/jimmunol.198.supp.222.22" @default.
- W4313384997 hasPublicationYear "2017" @default.
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