Sphingosine 1-Phosphate 1 and TLR4 Mediate IFN-β Expression in Human Gingival Epithelial Cells

摘要: IFN-beta production is a critical step in human innate immune responses and primarily controlled at the transcription level by highly ordered mechanisms. can be induced pattern-recognition receptors such as TLR4. S1P1 G protein-coupled receptor, which has high affinity for sphingosine 1-phosphate (S1P). Although many of signaling pathways leading to expression have been identified characterized, it still unclear how regulated primary gingival epithelial cells (HGECs). In this study, we demonstrate that TLR4, acting unison, play an important role protein mRNA HGECs. We both IFN-inducible protein-10 (CXCL-10) significantly up-regulated LPS S1P or specific agonist. This enhanced response attenuated HGECs small interfering RNA knockdown either TLR4 S1P1. Moreover, show triggering results increased receptors. Furthermore, found IFN-regulatory factor 3 activation was maximized through PI3K. Our data increases S1P1, PI3K enhancement increase cells. The functional association between receptor demonstrates novel mechanism regulation CXCL-10