简介：Directionalmigrationofleukocytesisindispensabletoinnateimmunityforhostdefense.However,recruitmentofleukocytestoasiteoftissueinjuryalsoconstitutesaleadingcauseforinflammatoryresponses.Mechanistically,itinvolvesacascadeofcellulareventspreciselyregulatedbytemporalandspatialpresentationofarepertoireofmoleculesinthemigratingleukocytesandtheirsurroundings(microenvironments).HereIwillsummarizetheemergingevidencethathasshedlightsontheunderlyingmolecularmechanismfordirectionalmigrationofleukocytes,whichhasguidedthetherapeuticaldevelopmentforinnovativeanti-inflammatorymedicines.

简介：ImmunizationwithinactivatedautoreactiveTcellsmayinduceidiotypeanti-idiotypicreactionstodepleteautoreac-tireTcells,whichareinvolvedinautoimmunediseases.However,itisunknownwhetherattenuatedactivatedhealthyautologousT-cellimmunizationcouldincreaseanti-tumorimmuneresponses.Tothisend,C57B1/6micewereimmunizedwithattenuatedactivatedautologousTcells.Thesplenocytesfromimmunizedmiceshowedahigherproliferativeabil-itythanthatfromnaivemice.ThespecialphenotypeanalysisshowedthatthereweremoreCDS+TcellsandCD62L+Tcellsinimmunizedmiceafter24hofculturewith10%fetalcalfserumcompletemediuminvitro(P<0.01).TheseresultsdemonstratedthatthisimmunizationmayactivateTcellsinvivo.Furthermore,thesplenocytesfromimmunizedmicerevealedresistancetoactivation-inducedcelldeath(AICD)invitro.TofurtherstudytherelativegenesthatareresponsibleforthehigherproliferationandresistancetoAICD,theexpressionofFas/Fasligand(FasL)andGADD45βwasmeasuredbyreal-timePCR.TheresultsindicatedthatGADD45βtranscriptionwashigherinthesplenocytesfromimmunizedmicethanthatinthenaivemice.Inaddition,theFasexpressionshowedaparallelhigher,butFasLdidnotchangeobviously.Toinvestigatethebiologicfunctionsinducedbyimmunizationinvivo,atumormodelwasestablishedbyEL-4tumorcellinoculationinC57/B1mice.MicereceivingautologousT-cellimmunizationhadsignificantlyinhibitedtumorgrowthinvivo(P<0.01).ThisstudyimplicatedthatimmunizationwithattenuatedactivatedautologousTcellsenhancesanti-tumorimmuneresponsesthatparticipateintumorgrowthinhibition.

简介：<正>WeandothershavefirmlyestablishedthatsurfaceIgMreceptor(sIgM-R)crosslinkingwithantibodiestotheiheavychain(anti-i)leadstogrowtharrestandapoptosisinaseriesofwellcharacterizedB-celllymphomas.Thisrequiresablationofc-Mycproteinexpressionandtheconcomitantinductionofthecyclin-dependent-kinaseinhibitor,p27Kip1.Thesignalingmechanismsregulatingc-Mycandp27Kip1proteinexpressionarepoorlyunderstood.However,werecentlyestablishedthatsIgM-Rmediateddown-modulationofthePI-3Kpathwaydirectlyaffectedc-Mycandp27Kip1expressionandaccuratelypredictedgrowtharrest