Tostudytheroleofnaturalkiller(NK)cellsinTcellrecruitmentinmurineliverinfectedwithvirus,micewereintravenouslyinjecteddailywithanti-NK1.1^+antibodytodepleteNKcells.Lymphocytesinthelivertissueofmiceinfectedwithtype5adenovirusdepletedintheE1andE3regionswereassessedbyfluorometricactivatedcellsorting(FACS).Ex-pressionofchemokineIP-10anditsreceptorCXCR3mRNAintheliver,hepaticlymphocytesandspleentissuewereexaminedbyreversetranscriptionpolymerasechainreaction(RT-PCR).Serumalmfineaminotransferase(ALT)wasmeasuredasanindicatorofliverinjury.Itwasfoundthatinfectionofadenovimsandanfi-Fasmonoclonalantibody(mAb)intomicecausedliverinjuryandhighexpressionofinterfemn-γinducibleprotein-10(IP-10)mRNAintheliver.Anfi-NK1.1^+mAb,whichwasintraperitoneallyinjectedintothemiceinfectedwithadenovirus,suppressesTcellrecruitmentandexpressionofIP-10mRNAinthehver.Slighterhverinjurywasalsoobserved.Afterviresinfection,expressionofCXCR3mRNAinspleenandhvertissuewasobservedatdifferenttime.TheresultssuggestedthatTcellrecruitmentwasinitiatedbyNKcelldependentchemokineIP-10,whichinducedactivatedTcellspriminginthespleentothehverofthemouse.NKcellsplayedakeyroleinTcellrecruitmentintheliverofmouseinfectedwithadenovims.
