In B cells, TLR ligation is important for their activation and, together with CD40, for their differentiation. TLR ligands are also strong promoters of regulatory B (Breg)-cell development, by enhancing the production of IL-10 and their capacity to induce tolerance. In inflammatory diseases, ...
Ligation of TLR2 by vers- ican: a link between inflammation and metastasis. Arch Med Res 2009; 40: 321-3.Wang W,Xu G L,Jia W D.Ligation of TLR2 by versican:a link between inflammation and metastasis[J].2009,40(04).Wang W, Xu GL, Jia WD, Ma JL, Li JS, Ge YS, Ren WH, ...
We set out to provide a comprehensive analysis defining differences in response to TLR ligation between human neonates and adults. In response to most TLR ligands, neonatal innate immune cells, including monocytes and conventional and plasmacytoid dendritic cells produced less IL-12p70 and IFN-伪 (...
underscores that molecules derived from other cell types significantly shape the B cell responses to TLR ligation. Trout peritoneal IgM+cells, uponin vivoexposure toE. colior VHSV, are shown to differentiate towards IgM-secreting cells, and at the same time these cells show decreased levels of MH...
Here we show that deficiency in β2 integrins (Itgb2/) causes hyperresponsiveness to TLR stimulation, demonstrating that β2 integrins inhibit signals downstream of TLR ligation. Itgb2/ macrophages and dendritic cells produced more IL-12 and IL-6 than WT cells when stimulated with TLR agonists ...
ligand activated dendritic cells have been described for TLR2, 3, 4, 7, and 9 ligands. In addition, TLR3 and 7 ligands indirectly increase tumor cell lysis by human γδ T cells, whereas ligation of TLR8 abolishes the suppressive activity of human tumor-infiltrating Vδ1 γδ T cells ...
After ligand ligation, these TLRs elicit the MyD88-dependent pathway to regulate inflammatory responses by activating NF-κB and AP-1. In pDCs, IRF7 is constitutively expressed and forms a signaling complex with MyD88, IRAK1 and IRAK4. In response to ligand stimulation, IRF7 is phosphorylated...
许多佐剂(包括tlr激动剂)与apc上的先天性免疫受体结合,诱导apc呈递抗原,产生细胞因子,并向抗原特异性cd8t细胞提供共刺激信号(1,2)。响应这些信号,cd8t细胞增殖并分化为能够杀灭表达其靶抗原的感染的或肿瘤细胞的ctl。另外,这种信号激活cd4t细胞,诱导其扩繁和分化为th1或th2t辅助细胞(3)。
The kind of stimulus has an impact on the response pattern following TLR ligation as well. TLR4 activation by Chlamydia heat shock protein 60 may trigger trophoblast death, even if LPS did not in the first trimester [27]. The varying downstream signaling events and distinct ways that various ...
The activity of the transcription factor NF-κB is enhanced by TLR stimulation as early as 15-30 minutes after TLR ligation, with subsequent cytokine production occurring 2 hours later [38, 39]. The most evident consequence of TLR stimulation is the induction of the inflammatory response. TLR ...