A Novel Dimeric Inhibitor Targeting Beta2GPI in Beta2GPIAntibody Complexes Implicated in Antiphospholipid Syndrome 英文参考文献.docVIP
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A Novel Dimeric Inhibitor Targeting Beta2GPI in Beta2GPIAntibody Complexes Implicated in Antiphospholipid Syndrome 英文参考文献
ANovelDimericInhibitorTargetingBeta2GPIin
Beta2GPI/AntibodyComplexesImplicatedin
AntiphospholipidSyndrome
AlexeyKolyada,Chang-JinLee,AlfredoDeBiasio,NataliaBeglova*
DepartmentofMedicine,BethIsraelDeaconessMedicalCenterandHarvardMedicalSchool,Boston,Massachusetts,UnitedStatesofAmerica
Abstract
Background: b2GPI is a major antigen for autoantibodies associated with antiphospholipid syndrome (APS), an
autoimmunediseasecharacterizedbythrombosisandrecurrentpregnancyloss.Onlythedimericformofb2GPIgenerated
byanti-b2GPIantibodiesispathologicallyimportant,incontrasttomonomericb2GPIwhichisabundantinplasma.
PrincipalFindings:Wecreatedadimericinhibitor,A1-A1,toselectivelytargetb2GPIinb2GPI/antibodycomplexes.Tomake
thisinhibitor,weisolatedthefirstligand-bindingmodulefromApoER2(A1)andconnectedtwoA1moduleswithaflexible
linker. A1-A1 interferes with two pathologically important interactions in APS, thebinding of b2GPI/antibody complexes
with anionic phospholipids and ApoER2. We compared the efficiency of A1-A1 to monomeric A1 for inhibition of the
bindingofb2GPI/antibodycomplexestoanionicphospholipids.Wetestedtheinhibitionofb2GPIpresentinhumanserum,
b2GPI purified from human plasma and the individual domain V of b2GPI. We demonstrated that when b2GPI/antibody
complexesareformed,A1-A1ismuchmoreeffectivethanA1ininhibitionofthebindingofb2GPItocardiolipin,regardless
of the source of b2GPI. Similarly, A1-A1 strongly inhibits the binding of dimerized domain V of b2GPI to cardiolipin
comparedtothemonomericA1inhibitor.Intheabsenceofanti-b2GPIantibodies,bothA1-A1andA1onlyweaklyinhibit
thebindingofpathologicallyinactivemonomericb2GPItocardiolipin.
Conclusions: Our results suggest that the approach of using a dimeric inhibitor to block b2GPI in the pathological
multivalentb2GPI/antibodycomplexesholdssignificantpromise.ThenovelinhibitorA1-A1maybeastartingpointinthe
developmentofaneffectivetherapeuticforantiphospholipidsyndrome.
Citation: Kolyada A, Lee C-J, De Biasio A, Beglova N (2010) A N
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