To function optimally,human blood natural killer(NK)cells need to communicate with other immune cells.Previously,it has been shown that NK cells communicate with 6-sulfo LacNAc dendritic cells(slanDCs),which are able ...To function optimally,human blood natural killer(NK)cells need to communicate with other immune cells.Previously,it has been shown that NK cells communicate with 6-sulfo LacNAc dendritic cells(slanDCs),which are able to stimulate NK cells in vitro.In this study,we investigated how slanDCs regulate the level of NK cell activation.The secretion of interleukin(IL)-1βby slanDCs during coculture with NK cells increased as a result of signaling via intercellular adhesion molecule-1 on slanDCs following its interaction with lymphocyte functionassociated antigen-1 on NK cells.IL-1βinduced the expression of Fas receptor(CD95)on NK cells.The binding of Fas ligand(CD178)to CD95 induced the apoptosis of activated NK cells.Moreover,IL-1βalso induced increased cyclooxygenase-2 expression in slanDCs,which in turn enabled the cells to secrete prostaglandin(PG)-E2.Consequently,PGE2 acted as a suppressing agent,tuning down the activation level of NK cells.In summary,IL-1βlimits the level of NK cell activation by inducing apoptosis and suppression as a homeostatic regulatory function.展开更多
基金grants from the Deutsche Forschungsgemeinschaft(DFG):SFB738/A5,Deutsche Zentrum für Infektionsforschung(DZIF):TTU 04.802,Hannover Biomedical Research School(HBRS),REBIRTH Cluster of Excellence and Niedersächsische Krebsgesellschaft e.V.
文摘To function optimally,human blood natural killer(NK)cells need to communicate with other immune cells.Previously,it has been shown that NK cells communicate with 6-sulfo LacNAc dendritic cells(slanDCs),which are able to stimulate NK cells in vitro.In this study,we investigated how slanDCs regulate the level of NK cell activation.The secretion of interleukin(IL)-1βby slanDCs during coculture with NK cells increased as a result of signaling via intercellular adhesion molecule-1 on slanDCs following its interaction with lymphocyte functionassociated antigen-1 on NK cells.IL-1βinduced the expression of Fas receptor(CD95)on NK cells.The binding of Fas ligand(CD178)to CD95 induced the apoptosis of activated NK cells.Moreover,IL-1βalso induced increased cyclooxygenase-2 expression in slanDCs,which in turn enabled the cells to secrete prostaglandin(PG)-E2.Consequently,PGE2 acted as a suppressing agent,tuning down the activation level of NK cells.In summary,IL-1βlimits the level of NK cell activation by inducing apoptosis and suppression as a homeostatic regulatory function.
