摘要
IL-16isaligandandchemotacticfactorforCD4+Tcells.IL-16inhibitstheCD3mediatedlymphocyteactivationandproliferation.TheeffectsofIL-16onthetargetcellsaredependentonthecelltype,thepresenceofco-activatorsetc.TounderstandtheregulationfunctionandmechanismofIL-16ontargetcells,weuseda130a.a.recombinantIL-16tostudyitseffectsonthegrowthofJurkatTleukemiacellsinvitro.WefoundthattherIL-16stimulatedtheproliferationofJurkatcellsatlowdose(10^-9M),butinhibitedthegrowthofthecellsathigherconcentration(10^-5M).Resultsshowedthat10^-5MofrIL-16treatmentinducedanenhancedapoptosisinJurkatcells.ThetreatmentblockedtheexpressionofFasL,butup-regulatedthec-mycandBidexpressioninthecells.Pre-treatmentofPKCinhibitororMEK1inhibitormarkedlyincreasedordecreasedtherIL-16inducedgrowth-inhibitingeffectsonJurkatcells,respectively.TheresultssuggestedthattherIL-16mightbearegulatorforthegrowthorapoptosisofJurkatcellsatadose-dependentmanner.Thegrowth-inhibitingeffectsofrIL-16mightbeFas/FasLindependent,but,associatedwiththeactivationofPKC,up-regulatedexpressionofc-MycandBid,andtheparticipationoftheERKsignalpathwayinJurkatcells.
出版日期
2002年05月15日(中国期刊网平台首次上网日期,不代表论文的发表时间)