Alternate Splicing of Interleukin-1 Receptor Type II (IL1R2) In Vitro Correlates with Clinical Glucocorticoid Responsiveness in Patients with AIED 英文参考文献.docVIP

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Alternate Splicing of Interleukin-1 Receptor Type II (IL1R2) In Vitro Correlates with Clinical Glucocorticoid Responsiveness in Patients with AIED 英文参考文献.doc

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Alternate Splicing of Interleukin-1 Receptor Type II (IL1R2) In Vitro Correlates with Clinical Glucocorticoid Responsiveness in Patients with AIED 英文参考文献

AlternateSplicingofInterleukin-1ReceptorTypeII (IL1R2)InVitroCorrelateswithClinicalGlucocorticoid ResponsivenessinPatientswithAIED AndreaVambutas1,2*,JamesDeVoti2,ElliotGoldofsky1,MichaelGordon1,MartinLesser2, VincentBonagura2 1The Apelian Cochlear Implant Center, Department of Otolaryngology, North Shore-LIJ Health System, Clinical Teaching Campus for the Albert Einstein College of Medicine,NewHydePark,NewYork,UnitedStatesofAmerica,2TheFeinsteinInstituteforMedicalResearch,Manhasset,NewYork,UnitedStatesofAmerica Abstract Autoimmune Inner Ear Disease (AIED) is poorly characterized clinically, with no definitive laboratory test. All patients suspected of having AIED are given glucocorticoids during periods of acute hearing loss, however, only half initially respond,andstillfewerrespondovertime. WehypothesizedthatAIEDisasystemicautoimmunediseasecharacterizedby dysfunctionalperipheralbloodmononuclearcells(PBMC)responsestoauniquecochlearantigen(s).Totestthishypothesis, we examined end-stage AIED patients undergoing cochlear implant surgery and compared autologous perilymph stimulatedPBMCfromAIEDpatientstocontrols.WedeterminedthatautologousperilymphfromAIEDpatientswasunable toinduceexpressionofalongmembrane-boundInterleukin-1ReceptorTypeII(mIL1R2)transcriptinPBMCascompared withcontrols,despitesimilarexpressionoftheshortsolubleIL1R2(sIL1R2)transcript(p,0.05).IL1R2isamoleculardecoy thattraps interleukin-1b(IL-1b)anddoesnotinitiatesubsequent signalingevents,thereby suppressinganinflammatory response.IL1R2transcriptlengthisregulatedbyalternatesplicing,andthemajorinhibitoryfunctionisattributedtothefull- length mIL1R2. In addition, IL1R2 expression is induced by dexamethasone. Separately, we prospectively examined patientswithneweronsetglucocorticoid-responsiveAIED.Immediatelypriortoclinicaltreatmentforacutedeteriorationof hearingthresholds,theirPBMCdemonstratedarobustinductionofmIL1R2inPBMCinresponsetodexamethasoneinvitro thatcorrelatedwithaclinicalresponsetopredniso