Inordertoclarifytheeffectsof17β-estradiol(E2)onnaturalkiller(NK)cellsandthepossiblyregulatorymechanisms,weobtainedhighlypurifiedandviableNKcellsfromC57BL/6Jmousespleenbyamagneticcellsorter(MACS).ThesecellsweretreatedwithE2andthentheircytotoxicityandproliferativecapacitywereexamined.TofurtherinvestigatethemechanismsontheeffectofE2onNKcells,expressionsofactivation-associatedmarkers(CD69,CD122)andinhibitoryreceptors(CD94,Ly49),andintracellularcytokineproductionwereanalyzed.Atlast,weperformedthecDNAmicroarraytoexplorethepossibleinvolvedgenes.WefoundthatE2couldsuppressNKcellcytotoxicityandproliferativecapacityinvitro.E2reducedNKcellcytotoxicityandproliferativecapacity,whichmaybethroughinfluencingthephenotypesandcytokineexpressionofNKcells,mainlyinvolvingCD94andIFN-γ.Furthermore,regulationofStat4,Fyn,Sh2d1a,Eat2,Cd244,Irf1,Runx1,Irf7,Irf5,EsrraandNr5a1genesmayberelatedtothecytotoxicity,proliferationandcytokineproductionofE2-mediatedpurifiedNKcells.
