Negative regulation of Toll-like receptor-mediated immune responses
By F. Liew, Damo Xu, E. Brint, Luke A. O'Neill. Nature reviews. Immunology, 2005
1,638 citations recorded by the source corpus.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/b796b8bcbbb6b92e7bfe1cd2bab641385c18c140
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In Immunology
Citations in the corpus
- Molecular Mechanisms That Influence the Macrophage M1–M2 Polarization Balance (2014, background): “Along the same lines, chronic signaling through the TLR4 pathway has been shown to induce various negative regulators like IRAK-M, ST2, SOCS1, short version of MyD88 (MyD88sh) (27, 28) and SHIPs (29).”
- Dendritic cells: translating innate to adaptive immunity. (2006, background): “Many additional inhibitory pathways for TLR signaling have also been identified (reviewed in [183]).”
- IL‐1, IL‐18, and IL‐33 families of cytokines (2008, background): “The Toll-like receptors (TLRs) detect pathogenassociated molecular patterns (PAMPs) from bacterial cell walls and nucleic acids and have been implicated in many human diseases (3).”
- Macrophage death and defective inflammation resolution in atherosclerosis (2009, background): “Although this Review has focused on upstream mediators of inflammation resolution, complex negative feedback mechanisms at the transcriptional and translational levels are crucial sequelae of the inflammatory respons”
- Function of Nod‐like receptors in microbial recognition and host defense (2009, background): “The lack of cross-inhibition between TLR and Nod1 ⁄ Nod2 signaling is consistent with observations that TLR tolerization targets upstream components of the TLR pathway that are not involved in Nod1 ⁄Nod2 signaling (95).”
- Ligand-induced endocytosis of the pattern recognition receptor FLS2 in Arabidopsis. (2006, background): “Several negative regulators of TLR signaling have been recently described, which function on different levels, for example, through extracellular PAMP scavengers, cytosolic adapter proteins, or transmembrane protein regulators, or by down-regulation of TLR expression (Liew et al. 2005).”
- Transcriptional control of the inflammatory response (2009, background): “The first category consists of regulators that inhibit signal transduction by TLRs and other inflammatory pathways, and includes A20 , ST2 , IL-1R-associated kinase M ( IRAKM ) and suppressor of cytokine signalling (SOCS) protein”
- miR-146a is a significant brake on autoimmunity, myeloproliferation, and cancer in mice (2011, background): “Decades of intense study have uncovered multiple layers of innate immune regulation, from soluble receptors to inducible intracellular protein regulators (Liew et al., 2005).”
- Transition from inflammation to proliferation: a critical step during wound healing (2016, background): “Interestingly, most of these inhibitors are induced through TLR activation, thus acting through a negative-feedback loop to limit or turn off the TLR signalling [122].”
- Resolution of inflammation: state of the art, definitions and terms (2006, background): “In effect, TLRs sow the seeds of their own destruction, and the role of negative regulators clearly indicates how robust the TLR system is.”
- Tolerance and M2 (alternative) macrophage polarization are related processes orchestrated by p50 nuclear factor κB (2009, background): “Other negative regulators of NF- B activation have been identified in disease and include the LPS-inducible splice variant of myeloid differentiation 88 (MyD88), termed MyD88s, the single Ig IL-1 receptor-related molecule (SIGIRR)/TIR8, ST2, IRAK-M, SOCS1 (9, 13), and the Src homology 2-containing i”
- Toll-like receptors on hematopoietic progenitor cells stimulate innate immune system replenishment. (2006, background): “Several negative regulators for TLR signaling have been reported that might work in a cell type dependent manner (Liew et al., 2005).”