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ISSN1838-904X

PROCEEDINGSOF

NEUROIMMUNOLOGYAUSTRALIA

Volume6 July2017

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ProceedingsofNeuroimmunologyAustralia

AcompanionjournaltotheworkshopofNeuroimmunologyAustralia

EDITORSDavidABrownTheWestmeadInstituteforMedicalResearch.TheUniversityofSydney

StefanBlumUQCentreforClinicalResearch.TheUniversityofQueensland

JudithMGreerUQCentreforClinicalResearch.TheUniversityofQueensland

FabienneBrilotKidsResearchInstituteTheChildren’sHospitalatWestmead.TheUniversityofSydney

ISSN1838-904X

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ProceedingsofNeuroimmunologyAustraliaVolume6,July2017

Abstractsofpresentations(Presentersbyalphabeticalorder)

ChristineBundell-GANGLIOSIDEANTIBODYTESTINGINACLINICALCOHORTUSINGANEXTENSIVEGANGLIOSIDEPANEL-POSTERAakankshaDixit-PROTECTIONAGAINSTRELAPSESOFDISEASEINAMOUSEMODELOFMULTIPLESCLEROSISBYAPARASITE-DERIVED68-MERPEPTIDE

JudithGreer-CANAUTOIMMUNETHYROIDDISEASECAUSEAUTOIMMUNEATTACKINTHECNS(ANDVICE-VERSA)?Joseph Angelo Lopez-VALIDATING A MOG-ANTIGEN TETRAMER FOR DETECTINGMOG-SPECIFIC MEMORY B CELLS IN PATIENTS WITH CNS DEMYELINATINGDISORDERSEmilyMathey-AUTOANTIBODYRESPONSESTONODALANDPARANODALANTIGENSINCHRONICINFLAMMATORYNEUROPATHIESMasturaMonif-THE DISTINCTIVE ROLE OF MALT1 IN TOLERANCE ANDAUTOIMMUNITYDeeptiPilli-TCELLACTIVATIONBYTHEDOPAMINE-2RECEPTORINCHILDRENWITHMOVEMENT&PSYCHIATRICDISORDERSSudarshini Ramanathan-THE CLINICAL COURSE, THERAPEUTIC RESPONSES, ANDOUTCOMESINRELAPSINGMOGANTIBODY-ASSOCIATEDDEMYELINATIONAndrewSwayne-MANAGINGMYASTHENIAGRAVISWITHLOW-DOSERITUXIMAB:ACASESERIESANDREVIEWOFTHELITERATUREVanessaX.Tan-KYNURENINEPATHWAYMETABOLITESASPROGRESSIONMARKERSFORMNDMarc Ruitenberg-INTRAVENOUS IMMUNOGLOBULIN (IVIG) AS ANIMMUNOMODULATORYTHERAPYFORACUTESPINALCORDINJURYAliciaWilson-TH17CELLSAREDYSREGULATEDINTHEABSENCEOFDOCK8-POSTER-POSTER

Alicia Zou-INVESTIGATING THE DIVERSITY AND IMMUNOREACTIVITY OFRECOMBINANT ANTI-MOG ANTIBODIES ASSOCIATED WITH CENTRAL NERVOUSSYSTEMDEMYELINATINGDISEASES

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IntroductiontotheProceedingsofNeuroimmunologyAustralia

NeuroimmunologyAustraliaisabodythatwasformedin2010,with the aim of providing a forum for discussion of immune-mediated diseases of the brain, spinal cord, peripheral andautonomicnerves,theneuromuscularjunctionandmuscles.The members of Neuroimmunology Australia come from thefieldsofclinicalimmunology,basicimmunology,neurologyandneurosciences,andfromhospitals,diagnostic laboratoriesanduniversities.Theintentionistoprovideameetingwheretherecanbetrueinter-disciplinaryinteraction.ThefirstmeetingwasheldinBrisbanein2010,onthetopicof“Antibody-mediated Neurological Disease”. The range ofdiseases that were discussed was wide - ranging frommyastheniagravistoschizophrenia.Subsequentmeetingshavealso been held in Brisbane and Sydney in April 2011, August2012,July2014,July2015,August2016,andnowinJuly2017.TheProceedingsofNeuroimmunologyAustraliaispublishedtoprovide a permanent record of the work presented at themeetingsofNeuroimmunologyAustralia.TheproceedingshavebeenpublishedsincethesecondyearoftheNeuroimmunologyAustraliaannualscientificmeeting.

DavidABrownPresident,

NeuroimmunologyAustralia

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NIA2017PlenarySpeakers(alphabeticalorder) ProfessorDavidBrown,WestmeadMedicalResearchInstituteDavidBrowngraduated inMedicinefromUniversityofNSWin1989.Hetrained inclinicalimmunologyandimmunopathologyandwasawardedanFRACPandFRCPAin2000. In 2003, he completed a PhD research degree after which he undertookfurther post-doctoral studies at The Salk Institute for Biological Sciences, USA inneuroanatomy and neuroinflammation. He returned to Australia in 2006 and hasheaded his research group investigating CNS immunoregulation. He is Director ofImmunopathology at Pathology West, ICPMR and Heads the Laboratory ofNeuroinflammation at The Westmead Institute for Medical Research where hecontinues his research into CNS immunoregulation and the immune basis forPsychiatric disorders. He is president of Neuroimmunology Australia and isorganizing the International Society forNeuroimmunology Congress in Brisbane in2018.HealsoservesontheboardofTheInternationalSocietyofNeuroimmunology.ProfessorIainL.Campbell,UniversityofSydneyIain Campbell obtained his doctoral degree from the University of Sydney. Aftershort postdoctoral periods in Britain and Sweden, he returned to the RoyalMelbourneHospitalin1982astheinauguralD.W.KeirresearchfellowworkingwithProfessorLenHarrisonintheEndocrinelaboratory.In1985,hemovedtotheBurnetClinicalResearchUnitoftheWalterandElizaHallInstitute.HeleftAustraliain1989todoasabbaticalat theScrippsResearch Institute inLa Jolla,SanDiego,USAandthat iswherehe remained forover14 years as aNIH-fundedbiomedical researchscientistandaProfessorintheDepartmentofNeuropharmacology.IainreturnedtoAustralia in2004totakeontheroleasChairofMolecularBiology intheSchoolofMolecularBioscienceattheUniversityofSydney.From2011-2016hewastheHeadof the School of Molecular Bioscience. The overall goal of Iain’s research is tounderstandthemolecularandcellularmechanismsunderpinninghostdefenceandimmunoinflammatory processes that contribute to disease in the central nervoussystem.Heisauthor/co-authortoover250publicationsandhasacurrenth-indexof64.ProfessorGeorgesGrau,UniversityofSydneyImmunopathologyofmicrovascular lesions, particularly of cerebral andpulmonarycomplicationsofinfectiousandauto-immunediseases,especiallyincerebralmalaria,septic shock and multiple sclerosis. Analysis of the cellular and molecularmechanismsoftheinteractionsbetweenmicrovascularendothelialcellsandcellsoftheimmunesystem.Experienceinvariousinvivoandinvitroexperimentalsystemsas well as in clinical studies.More recently, focus on the neurovascular lesion ofmurineandhumancerebralmalaria,usingco-culturemodelsystemsinvolvingbrainendothelium, P. falciparum-infected erythrocytes, as well as circulating cells,particularlyplateletsandmonocytes.ProfessorGeorgesGrau obtained aMD from theUniversity of Liège and a Privat-Docent from the University of Genève. He has been the Chair of VascularImmunology at the University of Sydney since 2006. Since 1979, his research hasfocused on immunopathological mechanisms of infectious diseases, notably in

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cerebral malaria, multiple sclerosis and septic shock, with particular emphasis oncytokinesandthemicrovascularendothelium.His invivo interventionstudies inmurinemodelscontributed to theelucidationofcytokine interactions leading to tissue injury, with particular attention to tumournecrosisfactor(TNF),whichhadimportantimplicationsforcelladhesionmoleculesinvariousmodelsofpathology. Inmulti-compartmentco-culturesystems involvinghuman endothelial cells, his group found that platelets can act as effectors ofcytokine-induced microvascular damage. His team also demonstrated thatmembrane microparticles, released by several cell types, profoundly alterendothelialintegrityandtherebycanbecrucialelementsinimmunopathology.His 359papers (264peer-reviewed) havebeen citedover 27,000 times andhish-indexis83.AssociateProfessorJudithGreer,UniversityofQueenslandThe main focus of Judith Greer’s lab is diseases affecting the nervous system,particularlythoseinwhichtheimmunesystemplays(ormayplay)arole,particularlymultiple sclerosis (MS) and schizophrenia.HerMS research is directedparticularlytowards trying to identify brain components that are targeted by the immunesystem in peopleMS, in determining how immune responses within the nervoussystemrelate to thesymptomsexperiencedbypeoplewithMS,and indevelopingnewwaystospecificallyturnoffthedamagingimmuneresponsesinthebrain.Herwork on schizophrenia investigateswhether autoantibodies specific formuscarinicreceptorsplayfunctionalrolesinthedisease. ProfessorGillesGuillemin,MacquarieUniversityProfGuilleminhasbeenworkinginthefieldofNeuroinflammationformorethan24yearsandinthefieldoftryptophanmetabolismfor20years.Hehasbeenstudyingthe involvement of the tryptophan catabolism (via the kynurenine pathway) inhuman neurodegenerative diseases. He demonstrated the importance of thekynurenine pathway inmultiple sclerosis, Alzheimer's disease, amyotrophic lateralsclerosis, which opens numerous very promising research opportunities and hasimportant therapeutic potential. He also extended his research to other diseasessuchasdepression, autism,breast andbrain tumours.ProfGuilleminh-index is 50and current Researchgate score 46.61(top 2.5% scientist worldwide) is growingeverymonthwithpresentlymorethan300profileviewperweek.DrEmilyMathey,BrainandMindCentre,UniversityofSydneyDrEmilyMatheyisaresearchscientistintheNeuroinflammationLaboratoryattheBrain &Mind Centre at the University of Sydney. Dr Mathey did her PhD at theUniversity of Sydney followed by Postdoctoral Fellowships at the Max PlanckInstitute forNeurobiology,Martinsried,andUniversityofAberdeen,UKwheresheidentified novel autoantibody responses to neurofascin in patients with multiplesclerosis and tested thepathogenicityof auto-antibodies responses toneurofascinandcontactin2inanimalmodelsofMS.DrMathey’sresearchcontinuestofocusonidentifying novel autoantibody responses in patients with inflammatoryneuropathies,developingassaystoroutinelytestfortheseantibodiesinpatientseraandexaminingthepathogenicityoftheseresponsesinanimalmodels

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ProfessorPamelaMcCombe,UniversityofQueenslandDrMcCombeisaneurologistatRoyalBrisbaneandWomen'sHospitalandProfessorattheUniversityofQueenslandCentreforClinicalResearch.Sheworksinthefieldofneuroimmunology. Current interests include gender and pregnancy in multiplesclerosisandimmuneaspectsofmotorneuronediseaseandstroke.DrGilaMoalem-Taylor,UniversityofNewSouthWalesDrMoalem-Taylorgraduated with a PhD from theWeizmann Institute of Science,Israelin 2001.She was then awarded a Rothschild Postdoctoral Fellowship andmovedtoTheUniversityofCincinnatiMedicalCentreintheUSAwheresheworkedfor 2 years and developed an interest in the area of neuropathic pain. She thenmoved to the School of Medical Sciences at the University of New South Wales(UNSW) in Australia, where she was awarded the UNSW Vice-Chancellor’sPostdoctoral Fellowship (2004-2007), followed by the NSW OSMR CareerDevelopmentFellowshipundertheNSWSpinalCordInjuryandRelatedNeurologicalConditionsResearchGrantsProgram(2010-2013). In2014,shewasappointedasaSeniorLecturerintheDepartmentofPhysiology,TranslationalNeuroscienceFacility,School of Medical Sciences, UNSW.Since her PhD, Moalem-Taylor has workedprimarilyintheareaofneuroimmunology.Hercurrentresearchfocusesontheroleof immune cells and their mediators in neurodegeneration and neuropathic paincausedbyperipheralnerveinjury,autoimmunediseasesofthenervoussystemandspinalcordinjury.DrMarcRuitenberg,UniversityofQueenslandDr.MarcRuitenbergisthecurrentSpinalCureAustraliaResearchFellowandaSeniorLecturerinBiomedicalSciencesatTheUniversityofQueensland.Marcwasawardedhis PhD from the VU University Amsterdam in 2003, after having completed hisdoctoral research at The Netherlands Institute for Neuroscience. He relocated toPerth (WesternAustralia) that sameyear todohis post-doctoral trainingwith theWA Neurotrauma Research Program. He was recruited to The University ofQueenslandin2009whereheisnowtheHeadoftheLaboratoryforNeuralInjury&Repair.Akeyfocusofhisresearchistobetterunderstandtheroleofinflammationinacquiredcentralnervoussysteminjury,inparticulartraumaticspinalcord injury.Marc's laboratory is also engaged with the development of advanced magneticresonance-basedimagingtechniquestobetterdiagnoseandtreatspinalcordinjury.The ultimate goal of his research is to develop new and effective immune-modulatorytreatmentstoimproveoutcomesforneurotraumapatients.

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NIA2017Presenters(*posterpresentation*)*GANGLIOSIDEANTIBODYTESTING INACLINICALCOHORTUSINGANEXTENSIVEGANGLIOSIDEPANEL*ChristineBundell1,3,EKlinken1,2,AMcleanTooke1,2

1PathWestLaboratoryMedicine,QEIIMedicalCentre,Nedlands2DepartmentofClinicalImmunology,SirCharlesGairdnerHospitalQEIIMedicalCentreNedlands3 School of Biomedical Sciences, University of Western Australia, Crawley, Western AustraliaImmunemediatedperipheralneuropathiesmaybeassociatedwiththepresenceofautoantibodies that react to gangliosides. Although the diagnosis of autoimmuneneuropathies is based primarily on clinical evaluation and electrophysiologicalstudies, detection of ganglioside antibodies may provide useful additionalinformation to support the diagnosis. The reported frequency of some of theseantibodiesranges fromadetectable IgMGM1antibody in30-40%ofpatientswithmultifocalmotorneuropathytoverysmallnumbers(2positivecasesintheliteratureonly)forGM4antibodies.Clinical samples from229 consecutive patientswith a first request for gangliosideantibodieswere testedontheGenericAssays (GA;Germany) immunoblot.TheGAassay covers a broad rangeof ganglioside antibodies of both IgG and IgM classes:GD1a, GD1b, GD2, GD3, GM1-4, GQ1b, GT1a, GT1b. Requests came from similarnumbersofmalesandfemales(M:F120:109).Themeanageofmalesandfemaleswere58and53years respectively (SD=18forbothgroups).Gangliosideantibodieswere detected in 23% (n=51) of the patients. A single ganglioside antibody wasdetectedinn=21,2antibodiesinn=18,3antibodiesinn=4,4antibodiesinn=4and>4 antibodies in n=4 cases. Of the 4 cases with >4 antibodies detected, 3 had aclinicaldiagnosisofMillerFisherSyndromewithbothIgGGT1aandGQ1bdetected.Of the 18 that had a positive IgG GT1a, 14 had a concurrent positive IgG GQ1bantibody. Of these, 12 had a clinical diagnosis of Miller Fisher Syndrome.Anti-gangliosides may be seen in a significant proportion of patients referred fortestingforautoimmuneneuropathy.Multipleantibodypositivitywasseenin59%ofpositivepatientswith somepatientshavinga largenumberofpositiveantibodies.The concurrent detection of IgGGQ1b andGT1a antibodies is consistentwith thereportedcrossreactivitybetweenthesetwogangliosides.Inourcohort,IgGGD2andGD3wereonlydetectedinassociatedwithotherspecificities(inallcasesIgGGT1aand GQ1b). Further studies of larger cohorts of well-defined autoimmuneneuropathy patients are needed to determine the diagnostic accuracies of theseantibodies.

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PROTECTIONAGAINST RELAPSESOF DISEASE IN AMOUSEMODELOFMULTIPLESCLEROSISBYAPARASITE-DERIVED68-MERPEPTIDEAakankshaDixit1,JudithGreer1,SheilaDonnelly21UniversityofQueenslandCenterforClinicalResearch,UniversityofQueensland,Brisbane,Australia2TheSchoolofLifeSciences,UniversityofTechnologySydney,Sydney,AustraliaHelminths(parasiticworms)canexertprotectiveeffectsonautoimmunediseasesbymodulatingthetypeofimmuneresponse,anddeliberateinfectionwithhelminthsisbeingexploredasapotential therapeuticstrategyforautoimmunity.However, theuseoflivehelminthsastherapeuticagentsforautoimmunediseasehasanumberofdrawbacks,and itwouldbepreferable to identifyanduse the immunomodulatorycomponents of the helminths. Previously it has been shown that theimmunomodulatory activity of the liver fluke Fasciola hepatica resides in itsexcretory-secretory products (FhES), and further analysis of FhES has identified 3major components: an 68 amino acid alpha helical cathelicidin-like peptide(FhHDM1),a cathepsinL-cysteineprotease (FhCL1),andperoxiredoxin (FhPrx).Wehave found that FhHDM1 is themost effective at preventing development of theexperimentalautoimmuneencephalomyelitis(EAE)modelofmultiplesclerosis(MS).Inthecurrentstudy,wehaveinvestigatedthetherapeuticeffectsofFhHDM1whenit is given after the first attack of disease in a relapsing-remitting EAE model.FhHDM1significantly(p<0.0001)reducedtheoverallseverityofthediseaseandthenumberofrelapsescomparedtomicetreatedwithvehiclealone.Theeffectswerelong-lasting, withmice continuing to show benefits for up to 70 days following asinglecourseofFhHDM1treatment.Preliminary investigationofthemechanismofactionofFhHDM1suggeststhatit isnotaffectingtheadaptivearmoftheimmuneresponse, but is exerting significant effects by modulation of innate pro-inflammatory immuneresponsesandby limitingegressof immunecellsacrosstheglia limitans.Thedatasuggest that thisparasite-derivedpeptidehaspotentialasanoveltreatmentforpatientswithMS.

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CANAUTOIMMUNETHYROIDDISEASECAUSEAUTOIMMUNEATTACKINTHECNS(ANDVICE-VERSA)?JudithMGreer1,SimonBroadley2,3,MichaelPPender4,51CentreforClinicalResearch,TheUniversityofQueensland,Brisbane,QLD2SchoolofMedicine,GriffithUniversity,Southport,QLD3DepartmentofNeurology,GoldCoastUniversityHospital,Southport,QLD4FacultyofMedicine,TheUniversityofQueensland,Brisbane,QLD5DepartmentofNeurology,RoyalBrisbaneandWomen’sHospital,Brisbane,QLDSeveral lines of evidence suggest a definite and unique link between CNSdemyelinating diseases and autoimmune thyroid diseases (AITD). Somemoleculestargetedbythe immunesysteminAITDhaverelatedfamilymembersexpressedintheCNS.Oneexampleisthethyroid-stimulatinghormonereceptor(TSHR),presentin the thyroid, and the related molecule leucine-rich repeat-containing G-proteincoupledreceptor4 (LGR4),which isexpressed in thebrainstemandspinalcord. InthecurrentstudyweinvestigatedimmunoreactivitydirectedagainstTSHRandLGR4,HLA type and other features of disease in 44 patients with co-existing CNSdemyelinating disease and AITD (28 hypothyroid and 16 hyperthyroid patients),comparedtopatientswithmultiplesclerosisaloneorhealthyindividuals.Patients with co-existing AITD and CNS demyelinating disease were almostexclusivelyfemale(43/44)andhadprominentspinalcord involvementasthemainneurological finding. Patients with hyperthyroid disease weremore likely to havehadAITDpriortotheonsetofCNSdiseasethanwerepatientswithhypothyroidism(67%vs32%).BloodandDNAwerecollectedandtested forHLAtype,and for theresponse of T cells and antibodies to TSHR, LGR4 and myelin proteolipid protein(PLP).TheHLAmoleculescarriedbyindividualswithCNSdemyelinatingdiseaseandAITDdiffered frombothotherMSpatients andhealthy individuals,with themostdifferent group being patients with co-existing autoimmune hyperthyroidismpreceding the onset of CNS demyelinating disease. Patients with co-existing CNSdiseaseandAITDshowedlessTcellreactivitythanpatientswithMSalonetomyelinproteolipid protein (PLP). Furthermore, patients with co-existing CNS disease andhyperthyroidismshowedelevatedlevelsofantibodyandTcellreactivitytoLGR4andTSHRcomparedtoothergroups.We suggest that autoreactive immune cells cross-reactive against related antigenspresent in the thyroid and the spinal cord underlie the pattern of lesiondevelopment in theCNS inpatientswithco-existingAITDandMS.Furthermore, inpatients with hyperthyroidism, CNS disease may be a direct consequence ofspreading of disease from the thyroid to the CNS, due to immune cross-reactivitytargettingTSHRandLGR4.Theremaybesimilar linksbetweenotherantigens thatareexpressedinthethyroidandCNS.

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VALIDATING A MOG-ANTIGEN TETRAMER FOR DETECTING MOG-SPECIFICMEMORYBCELLSINPATIENTSWITHCNSDEMYELINATINGDISORDERSJoseph Angelo Lopez1, Fiona Tea1, Deepti Pilli1, Joseph Angelo Lopez1, Alicia Zou1,

SudarshiniRamanathan1,VeraHarb1,FionaLee1,RussellDale1,FabienneBrilot11BrainAutoimmunityGroup,InstituteforNeuroscienceandMuscleResearch,KidsResearchInstitute,The Children’s Hospital at Westmead, Discipline of Child and Adolescent Health, Sydney MedicalSchool,UniversityofSydney,Sydney,AustraliaAutoantibodies againstmyelin oligodendrocyte glycoprotein (MOG) are found in asubsetofpatientswithdemyelinatingdisordersofthecentralnervoussystem(CNS)andareinstrumentalindistinguishingMOGantibody-associateddemyelinationfromother demyelinating disorders such as multiple sclerosis. Recent literature hashighlighted the importance of the protein conformation of MOG in anti-MOGantibodydetectionandhasdemonstratedthatpathogenicanti-MOGantibodiesonlyrecognise MOG in its native conformation. The detection and characterisation ofMOG-specificmemoryBcellsindemyelinatingpatientsremainsunexplored.Firstly,weaimedtodetectanti-MOGantibodies intheserumofpatientswithCNSdemyelination.Secondly,weaimed to investigate thebindingofpatientanti-MOGantibodies to the StrepTactin-tagged extracellular Ig-like domain of human MOG(hMOG1-117).Anti-MOG antibody detection in serum samples was performed on a prospectivecohortof71adultpatientswithdemyelinatingdisordersusingalivecell-basedflowcytometry assay. 4/71 (6.3%) adult patients were seropositive for anti-MOGantibodies,whereasallcontrolswereseronegative(0/24,0%).Next,ahMOG1-117-coated enzyme-linked immunosorbent assay (ELISA) was performed to investigateanti-MOG antibody binding to hMOG1-117.We tested 12 adult controls, 12 anti-MOGantibodynegativepatients (n=12 fromprospective cohort)and12anti-MOGantibodypositivepatients(n=4fromprospectivecohort;n=8biobank-storedserumsamples tested previously). Preliminary findings demonstrated that anti-MOGantibodies from4/12 (33.3%) seropositivepatientswereable tobindhMOG1-117,while2/12(16.7%)seronegativepatientsand0/12(0%)controlsbound.AduplicateELISA was performed on a StrepTactin-coated plate to investigate intermoleculareffects of the ELISA plate on hMOG1-117 conformation. 6/12 (50%) seropositivepatientswere able to bind hMOG1-117 on a StrepTactin-coated plate,while 1/12(8.3%)seronegativepatientsandnoneofthecontrols(0/12,0%)bound,suggestingthatintermolecularinteractionsbetweentheELISAplateandhMOG1-117mayhaveaneffecton its conformationwhich coulddecrease the sensitivityof theantibodybinding assay. Deciphering the importance of conformation in anti-MOG antibodybindingwillassistoptimizationofpatientdiagnosisandtreatment.

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AUTOANTIBODYRESPONSESTONODALANDPARANODALANTIGENSINCHRONICINFLAMMATORYNEUROPATHIESEmilyMathey1,GargN1,ParkS1,NguyenT1,BakerS2,YukiN3,YiannikasC4,LinC5,SpiesJ6,GhaouiR7,BarnettM1,VucicS1,PollardJ1,KiernanM1

1BrainandMindCentre,UniversityofSydney,Sydney,Australia2 Department of Medicine, Physical Medicine and Neurology, Neuromuscular Disease Clinic,McMasterUniversity,Hamilton,Canada3MishimaHospital,Niigata,Japan4NorthernClinicalSchool,UniversityofSydney,Sydney,Australia5 School of Medical Sciences, Department of Physiology, Translational Neuroscience Facilities,UniversityofNewSouthWales,NewSouthWales,Australia6InstituteofClinicalNeurosciences,RoyalPrinceAlfredHospital,Sydney,Australia7NeurologyDepartment,RoyalAdelaideHospital,Adelaide,SouthAustralia,Australia.Autoantibodies to nodal/paranodal proteins have previously been reported inpatients with chronic inflammatory demyelinating polyneuropathy (CIDP) andmultifocalmotorneuropathy (MMN).However, theprevalence and significanceofnodalandparanodalantibodies insomegroupsofpatientswithimmune-mediatedneuropathiesremainsunclear.InthisstudywescreenedCIDPandMMNpatientsforantibodies to full length, human neurofascin-155 (NF155), contactin-1 (CNTN1),neurofascin-186(NF186)andgliomedinproteinsusingstandardELISA.7%(3/44)ofCIDP patients exhibited anti- NF155 antibodies and 7% (3/44) of CIDP patientsexhibitedanti-CNTN1antibodies. In contrast, neitherNF155norCNTN1antibodieswere found inMMN (N=15), anti-myelin associated glycoprotein positive patients(N=9),otherneuropathies (N=37)orhealthycontrols (N=28).Thepredominant IgGsubclassofNF155andCNTN1antibodieswasIgG4.Positiveresultswereconfirmedusingcell-basedassaysandindirectimmunofluorescenceonteasednervefibres.Wedidnotdetect IgGautoantibodiesagainst thesenodal/paranodalantigens inMMNpatients.ELISAassaysusingcommerciallyavailable, full lengthhumanproteinsareusefulfortheinitialscreeningofpatientsforIgGreactivitytoNF155andCNTN1.IgGsubclasscanthenbedeterminedandreactivityconfirmedusingcell-basedassaysorbindingtoteasednervefibres.CIDPpatientspositiveforantibodiesNF155orCNTN1make an important subgroup of patients and a standardized ELISA to screen forthese responses is a useful diagnostic tool. Moreover, early detection of anti-paranodalantibodiesinCIDPpatientsisakeystepindefiningdiseasesubtypesandwillguidethemosteffectivetreatmentstrategiestopreventdisruptionoftheaxo-glialjunctionandaxonaldegeneration.

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THEDISTINCTIVEROLEOFMALT1INTOLERANCEANDAUTOIMMUNITYMasturaMonif1,ChristopherA.Reid1,KimL.Powell1,KatherineJ.Drummond1,TerrenceJ.O’Brien1,DavidA.Williams1

1RoyalMelbourneHospital,UniversityofMelbourne,Melbourne,AustraliaNumerous neuroinflammatory conditions such as multiple sclerosis, andautoimmuneencephalitisshowenhancedexpressionofthepurinergicP2X7receptor(P2X7R)intheneuroinflammatoryfoci,whereincreasedmicroglialactivationisaco-existingfeature.WehavereportedthatsimpleP2X7R-overexpressionissufficientindrivingmicroglialactivationandproliferation.Onceactivated,microgliaareknownto release a number of bio-active substances that include the proinflammatorycytokine interleukin 1breta (IL-1beta). Previous studies have linked P2X7RstimulationtotheprocessingandreleaseofIL-1beta,butwhetherP2X7channelorP2X7Rporeisthepredominantentitydrivingthatreleaseisunknown.Usingprimaryhippocampal cultures, we reveal that the release of IL-1beta to be P2X7R poredependent. In addition,we found the trophic effects of P2X7R pore (in particularmicroglialactivationandproliferation) tobemediatedby IL-1beta. Inhibitionof IL-1betaproductionandinhibitionof itsfunction,resulted inasignificantdecrease inP2X7Rpore-inducedmicroglialactivationandproliferation.OurresultsindicatethatP2X7R stimulation is important in induction of microgliosis and inflammation andthat impairment of IL-1beta release due to blockade of P2X7R pore may be ofsignificant therapeutic benefit in neuroinflammatory and neurodegenerativeconditionswhereexcessiveIL-1betaisevident.

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T CELL ACTIVATION BY THE DOPAMINE-2 RECEPTOR IN CHILDREN WITHMOVEMENT&PSYCHIATRICDISORDERSDeepti Pilli1, Nese Sinmaz1, Sudarshini Ramanathan1, Fiona Tea1, Anthony DKelleher2, Tina.K Nguyen1, Vera Merheb1, Alicia Zou1, Joseph A Lopez1, Russell CDale1,FabienneBrilot11BrainAutoimmunityGroup,InstituteforNeuroscienceandMuscleResearch,KidsResearchInstitute,The Children’s Hospital at Westmead, Discipline of Child and Adolescent Health, Sydney MedicalSchool,UniversityofSydney,Sydney,Australia2TheKirbyInstituteforInfectionandImmunityinSociety,UNSWAustralia,Sydney,NSW,Australia,StVincent'sHospital,Sydney,NSW,AustraliaIntroduction&aim:Inasubsetofchildrenwithmovementandpsychiatricdisorders,thedopamine-2receptor(D2R)istargetedbyautoantibodies,reinforcingthecurrentautoimmune hypothesis of these brain diseases. Secretion of antibodies isdependentonaninterplaybetweenantibody-secretingBcellsandCD4+Tcells,bothspecific for the same antigen. However, as these D2R-specific T cells remainunexplored,we aim to identify and characterise them in childrenwithmovementandpsychiatricdisordersMethods: Rare activated D2R-specific CD4+T cells were detected via a sensitivewhole blood assay that assessed the co-expression of CD25 and CD134 followingstimulationwith a library of humanD2R peptides and positive stimulant controls,PHA,SEB,andtetanustoxoid(TT).PresenceofD2R-specificTcellswasconfirmedinchildren(n=19)andcontrols(n=18)ifthefrequencyofCD4+CD25+CD134+Tcellswasmore than 4 standard deviations over the control mean. To detect anti-D2Rantibodies in patient sera, a flow cytometery live cell-based assay was useddetermine antibody binding to transfected HEK293 cells expressing D2R. When adeltameanfluorescenceintensity(MFI)ofapatientwas3standarddeviationsabovethecontrolmean,theywereclassifiedasanti-D2Rantibodyseropositive.Results:TherewasasubgroupofpatientswhohadahigherfrequencyofactivatedCD4+CD25+CD134+T cells in response to D2R peptides aa51-75(1/19), aa156-195(2/19), aa206-265(1/18), aa306-365(1/19) andaa381-443(2/19).Nodifferencesin T cell activation against PHA, SEB, and TTwere observed between the cohorts(p<0.05).Ofthe19patients,3wereseropositiveforanti-D2Rantibodies.Conclusion:ActivationofD2R-specificCD4+Tcells isnotable inasubsetofchildrenwithmovementandpsychiatricdisorders.Exceptforonepatient,alargeproportionof theserespondersarenegative foranti-D2Rantibodies.ThissuggestsapotentialroleforautoreactiveTcellsthatisindependentofantibodiesintheseautoimmune-associateddisorders,therebyofferingwideroptionsfortreatment.

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THECLINICALCOURSE,THERAPEUTICRESPONSES,ANDOUTCOMESINRELAPSINGMOGANTIBODY-ASSOCIATEDDEMYELINATIONSudarshiniRamanathan1,MohammadS1,TantsisE1,NguyenT1,MerhebV1,Fung2,WhiteO3,BroadleyS4,5,Lechner-ScottJ6,VucicS7,HendersonA7,BarnettM8,ReddelS8,BrilotF1*,DaleRC1*onbehalfoftheAustralasianandNewZealandMOGStudyGroup*theseseniorauthorscontributedequally1BrainAutoimmunityGroup,InstituteforNeuroscienceandMuscleResearch,KidsResearchInstitute,The Children’s Hospital at Westmead, Discipline of Child and Adolescent Health, Sydney MedicalSchool,UniversityofSydney,Sydney,AustraliaObjective: We characterised the clinical course, treatment, and outcomes in 59patients with relapsing myelin oligodendrocyte glycoprotein (MOG) antibody-associateddemyelination.Methods: We evaluated clinical phenotypes, annualised relapse rates (ARR) priorand on immunotherapy, and expanded disability status scales (EDSS), in 216demyelinatingepisodesfrom33pediatricand26adultpatients.Results: The most common initial presentation was optic neuritis (ON) in 54%[bilateral(BON)32%,unilateral(UON)22%]inbothchildrenandadults,followedbyacutedisseminatedencephalomyelitis(20%)whichoccurredexclusively inchildren.ON was the dominant phenotype (BON 19% UON 34%) of all clinical episodes.107/224(48%)MRIshadnobrainlesions.Patientsweresteroidresponsivebut70%ofepisodestreatedwithoralprednisonerelapsed,especiallyatdoses<10mgdaily,within2monthsofcessation,andinassociationwithataperdurationlessthansixweeks. Immunotherapy, includingmaintenanceprednisone(P=0.0004), intravenousimmunoglobulin(IVIg),rituximab,andmycophenolate,allreducedmedianARRson-treatment.Treatmentfailurerateswerelowestwithmaintenanceprednisone(6%).Switching therapy in thosewho failed the first immunosuppressive agent reducedon-treatmentARR(P=0.03).59%ofpatientsexperiencedresidualdisability(averagefollow-up 60 months, visual loss in 25%). Three or more demyelinating episodeswereassociatedwithafollow-upEDSSof≥2(OR4.0,P=0.019).Conclusions: Relapsing MOG antibody-associated demyelination is stronglyassociatedwithON, is steroid responsivebutvulnerable to relapseonwithdrawal,and responsive to maintenance corticosteroids, IVIg, or immunosuppression.Increasingrelapsesleadtosustaineddisability.

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MANAGING MYASTHENIA GRAVIS WITH LOW-DOSE RITUXIMAB: A CASE SERIESANDREVIEWOFTHELITERATUREAndrewSwayne1,BaumannF1,PamelaMcCombe1,StefanBlum11CentreforClinicalResearch,UniversityofQueenslandBackground: B-Cell depletion therapy has a growing role in the management ofneurological diseases which are caused by a pathological immune response.Myasthenia gravis is one such disorder where antibodies are targeted againstproteinsrequiredforthefunctionoftheneuromuscularjunction.Rituximab(RTX),amonoclonal antibody against CD20 which depletes B cells, has been used in themanagementofagrowingnumberofpatientswithmyastheniagravis.Methods: A retrospective cohort studywas undertaken of patientswhohad beentreated with RTX in Brisbane with either acetylcholine receptor (AChR) ormusclespecifickinaseantibody(MuSK)positivemyastheniagravis.Intotal37patientswereincluded.InmostoftheseRTXwasadministeredin2divideddosesof500mgwithatotalof1gram.Monitoringwasconductedviaserialclinicalassessments,antibodytestingandflowcytometryofperipheralbloodBlymphocytes.Results: Across the cohort low dose RTX therapy was associated with peripheralblood B lymphocyte depletion, significant clinical improvement and reduction ofimmunosuppressive medications. The re-emergence of peripheral blood Blymphocytemarkerswaslinkedtoworseningofmyastheniagravissymptoms.Conclusion:TheuseofRTXatadoseof1graminthemanagementofpatientswithseveremyastheniagravisappearstobebeneficial.UsingserialanalysisofperipheralbloodBlymphocytesappearsusefulinguidingtheneedforfurtherRTXtherapy.

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KYNURENINEPATHWAYMETABOLITESASPROGRESSIONMARKERSFORMNDVanessaX.Tan1,AlainDuhamel2,ChaiK.Lim1,LauraBourbon1,VincentMeninger3,LucetteLacomblez3,MaevaKyheng2,PierreF.Pradat3,GillesJ.Guillemin11DepartmentofBiologicalSciences,FacultyofMedicineandHealthSciences,MacquarieUniversity,NewSouthWales,Australia2Université Lille, CHU Lille, EA 2694 - Santé Publique: Épidémiologie etQualité des Soins, F-59000Lille,France3DépartementofNeurology,ReferenceCenterforSLA,APHP,HospitalPitié-Salpêtrière,FranceA lack of suitable biomarkers for amyotrophic lateral sclerosis (ALS) hampersmonitoring of disease progression, furthermore, limits assessment of therapyefficiencyduringclinicaltrials.Inapilotstudyof66ALSpatientsfromaclinicaltrial,weusebiochemicalchromatographyanalysesto longitudinallycharacterizepatientserum Kynurenine Pathway (KP) profiles to determine if the KP is a suitablecandidate as an objective biomarker or prognostic indicator of ALS. to. The KP isactivatedby inflammation,andhasbeenshown tobedysregulated inALS [1], [2].Weshowthattogetherwithclinicaloutcomes,ALSFunctionalRatingScale(ALSFRS)and Manual Muscle Testing (MMT), KP metabolite 3hydroxyanthranilic acid isincreased over time (-1.20, -3.74, and -0.46 units over time). Tryptophan andKynurenine are both positively associated with ALSFRS; and Kynurenic Acid andQuinaldicAcidareassociatedwithMMT,indicatingthattheyaregoodcandidatesasbiomarkersforALS.Lastly,weshowthatneopterinisasignificantprognosticmarkerfor disease progression, with an increased neopterin level being associated withslower disease progression. These findings suggest that the KP may be a usefulmarker of disease progression and prognosis in ALS, and that further research tointegratetheKPwithotherknownbiomarkers,and largerdatasetsmayproduceaclinicallyrelevantandspecificbiomarkerforALS.TheKPshowspotentialfortrackingofdiseasedevelopmentinALS.Thiswillallowfora biochemical technique that will allow definitive monitoring of progression. ThisdatahasalsoallowedanindepthanalysisoftheKPchangesthroughthecourseofdisease. The role of immune modulating KP may be applied towards therapeuticconsiderationsbyusingKPalteringdrugsthatmayleadtonewtherapeuticoptionsforalleviatingtheclinicaleffectsofMND.[1]Y.Chenetal.,“TheKynureninePathwayandInflammationinAmyotropicLateralSclerosis,”Neurotox.Res.,vol.18,no.2,pp.132–142,2010.[2] J. Ilzecka, T. Kocki, Z. Stelmasiak, and W. A. Turski, “Endogenous protectantkynurenicacid inamyotrophic lateralsclerosis,”ActaNeurolScand,vol.107,no.6,pp.412–418,Jun.2003.

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HUMANMOGAUTOANTIBODIESRECOGNISEANEPITOPEATPROLINE42ANDTHISREACTIVITYREMAINSFionaTea1,DeeptiPilli1,JosephAngeloLopez1,AliciaZou1,SudarshiniRamanathan1,VeraHarb1,FionaLee1,RussellDale1,FabienneBrilot11BrainAutoimmunityGroup,InstituteforNeuroscienceandMuscleResearch,KidsResearchInstitute,The Children’s Hospital at Westmead, Discipline of Child and Adolescent Health, Sydney MedicalSchool,UniversityofSydney,Sydney,AustraliaAutoimmuneattacktothemyelinsheathofneuronsincentralnervoussystem(CNS)demyelinating diseases has piloted extensive study into autoantibodies targetingbrainmyelinproteins.Recently,autoantibodieswhichrecognisetheconformationalmyelin oligodendrocyte glycoprotein (MOG) have been clinically associated withsubsetsofCNSdemyelinatingdiseases,suchasbilateralopticneuritis.Weexaminedwhether the major epitope recognised by MOG autoantibodies from our adult(n=25) and paediatric (n=46) CNS demyelinating cohorts would be similar to thatpreviouslydescribedinchildren.WesubclonedandstablyexpressedinHEK293cellsahumanMOGmutant,MOGP42S,wheretheProlineatposition42wasmutatedtoSerine. After confirming surface expression of MOG P42S by flow cytometry andconfocal microscopy, we assessed sera MOG autoantibody binding using a flowcytometrylivecell-basedassay.ComparedtoMOGwild-type,80%(20/25)ofadult,and 76% (35/46) of paediatricMOG autoantibody-positive patients had a reducedbinding (<65%) to theP42SMOGmutant. Longitudinal analysisof threepaediatricandsixadultpatientsindicatedstableepitoperecognitionovertime.Takentogether,the Proline at position 42 of human MOG is a major conformational epitope inhuman MOG autoantibodies, and this binding remains stable overtime.Furthermore, as rodentMOGcontains a Serine at position42, our results supporttheassertionthathumanMOGautoantibodiesfailtobindrodentMOG.Thisspecies-specific epitope has major implications in future MOG autoantibody studies inrodent models. Greater characterisation of MOG autoantibodies will drivedevelopment of novel antibody therapies to improve patient management andtreatment.

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INTRAVENOUSIMMUNOGLOBULIN(IVIG)ASANIMMUNOMODULATORYTHERAPYFORACUTESPINALCORDINJURY BrennanFH1,KurniawanND2,ZuercherA3,KäsermannF3,ArumugamTV4,BastaM6,MarcRuitenberg1,6,7

1SchoolofBiomedicalSciences2CentreforAdvancedImaging3Research,CSLBehring,Bern,CH-3000,Switzerland4YongLooLinSchoolofMedicine,NationalUniversityofSingapore,117597,Singapore5BioVisionsInc.,Potomac,MD,20854,USA6TheQueenslandBrainInstitute,TheUniversityofQueensland,Brisbane,4072,Australia7Trauma,CriticalCareandRecovery,BrisbaneDiamantinaHealthPartners,Brisbane,4072,AustraliaTraumaticspinalcordinjury(SCI)elicitsimmediateneuralcelldeath,axonaldamageanddisruptionoftheblood-spinalcordbarrier,allowingcirculatingimmunecellsandbloodproteinsintothespinalparenchyma.TheacuteinflammatoryresponsetoSCIinvolves robust activation of the complement system, which contributes tosecondary injuryand impairsneurological recovery.Thisstudyaimedtodeterminewhether intravenous immunoglobulin (IVIg), an FDA-approved immunomodulatorytreatment, can attenuate complement activation products and improve recoveryfrom SCI.We addressed these questions by using functional testing, non-invasiveimaging,anddetailedpost-mortemanalysistoassessIVIg’stherapeuticefficacyinamousemodelofseverecontusiveSCI.OurresultsshowthatIVIgtherapyatclinicallyrelevant doses of 0.5-2 g/kg significantly improves functional and histopathogicaloutcomes from SCI, conferring protection against lesion enlargement,demyelination,andaxonaldegeneration.Thebenefitsof IVIgwerealsodetectablethrough non-invasive diffusion tensor imaging (DTI), with IVIg treatmentcounteractingtheprogressiveSCI-inducedincreaseinradialdiffusivity(RD)inwhitematter.Diffusionindicessignificantlycorrelatedwiththefunctionalperformanceofindividualmiceandaccuratelypredictedthedegreeofmyelinpreservation.Furtherexperiments revealed that IVIg therapy reduced complement activation andpresenceof phagocytically activemacrophages at the lesion site, providing insightintoitslikelymechanismsofaction.OurfindingshighlightthepotentialofusingIVIgas an immunomodulatory treatment for SCI, and the value ofDTI to assess tissuedamageandscreenfortheefficacyofcandidateinterventionstrategiesinpreclinicalmodelsofSCI,bothquantitativelyandnon-invasively.

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*TH17CELLSAREDYSREGULATEDINTHEABSENCEOFDOCK8-POSTER*AliciaWilson1,PadmajaTummala1,KatrinaL.Randall1,AnneBrüstle11TheJohnCurtinSchoolofmedicalResearch,AustralianNationalUniversityDedicatorofCytokinesis8(DOCK8)isaguanineexchangefactorhighlyexpressedintheimmunesystemandconnectedtocellpolarisation,proliferationandmigration.Multiple mouse models of DOCK8 deficiency show elevated numbers ofinflammatory Th17 cells opening the opportunity to investigate potential intrinsiceffectsofDOCK8deficiencyinTh17cells.AllDOCK8deficientmousemodelstestedshowed elevated CD4+ IL-17a producing cells, however no elevation of cytokinesproducedbyotherTcellsubsetswerealteredindictingaTh17cellspecificeffect.InvitroThelper celldifferentiationconfirmed that theelevatedTh17cellpopulationwasnotbasedonaThelpercellintrinsicdifferentiationdefectoralteredapoptosis.Th17cellsexpressednormal levelsof theTh17cell specificCCR6andwereable tomigratetowardschemokinegradientsininvitrotranswellmigrationassays.Wenextinvestigated if the increase inTh17cells ledtoan increasedpathology in theTh17cellmediateddiseaseexperimentalautoimmuneencephalomyelitis (EAE),amousemodel of autoimmune aspects of Multiple Sclerosis. Interestingly, homozygousDock8 mutant mice were found to have ameliorated disease despite increasedpercentagesofTh17cellsinthebloodinthesteadystate.AdoptivetransfersofTh1andTh17cells inEAEmicepointedtowardsaTh17cellspecificmigrationdefect inthe absence of functional DOCK8. We are currently investigating the molecularmechanismsunderlyingthiseffect.

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INVESTIGATING THE DIVERSITY AND IMMUNOREACTIVITY OF RECOMBINANTANTI-MOG ANTIBODIES ASSOCIATED WITH CENTRAL NERVOUS SYSTEMDEMYELINATINGDISEASESAliciaZou1,FionaTea1,DeeptiPilli1,JosephAngeloLopez1,SudarshiniRamanathan1,VeraHarb1,FionaLee1,RussellDale1,FabienneBrilot11BrainAutoimmunityGroup,InstituteforNeuroscienceandMuscleResearch,KidsResearchInstitute,The Children’s Hospital at Westmead, Discipline of Child and Adolescent Health, Sydney MedicalSchool,UniversityofSydney,Sydney,AustraliaBackground:Certaindisordersofcentralnervoussystem(CNS)neuromyelitisopticaspectrumdisorder(NMOSD),suchasbilateralorrelapsingopticneuritis,havebeenassociated with the presence of autoantibodies against myelin oligodendrocyteglycoprotein (MOG). The current understanding that a single majorimmunoreactivity exists in antibody-associated CNS disorders has been challengedby new findings of double autoantibody positivity in patients. As it stands, thediversityoftheantibodyrepertoireinpatientswithCNSdemyelinatingdiseasesandhowitevolveswithdiseaseisunknown.Methods:Tocharacterisetheautoantibodyrepertoireinanti-MOGantibody-positivepatients,pairedheavyandlightchainvariableregionswillbeamplifiedfromsingleBcellstobesubclonedintoexpressionvectorsandtransfectedintomammaliancellstoproducerecombinantmonoclonalantibodies(rAbs),whichcanthenbeanalysedfortheirbindingtoapanelofantigenictargets.Results: Flow cytometric analysis revealed that plasmablasts were more frequentthanplasmacells(0.65±0.4%vs0.00±0.0,respectively)intheperipheralbloodofhealthy controls, and were subsequently selected for single cell analysis.Amplificationofvariableheavyandlightchainsfromsingleplasmablastsusingone-stepRT-PCR revealed the lowefficiencyof thisprocess.Basedongelvisualisation,thevariable Igλchainwasamplified from4of18 (22%)singleplasmablasts,whichwas4timesmorefrequentthantheamplificationoftheIgκchain(1/18;5.56%).ThevariableIgHchainwasnotabletobevisualisedfromanysingle-sortedplasmablast.Atwo-stepRT-PCR,reported inthe literaturetobemoresensitivethanaone-stepRT-PCR for limitingconcentrationsofRNA,wasselected to improve theefficacyofimmunoglobulinchainamplification,andiscurrentlyundergoingoptimisation.Conclusion:Theproductionof rAbswill allow thecharacterisationofMOG-specificantibody response inpatientswithCNSdemyelinatingdisorders. Furthermore, thegenerationofabundantrAbscanbeusedtomodelfunctionalpathogeniceffectsininvitrocellularmodels.

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NeuroimmunologyAustraliawouldliketothankoursponsors:

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PARTICIPANTSName EmailaddressArnscheidtJohanna johanna.arnscheidt@sydney.edu.au

BeasleyShannon shannon.beasley@uq.edu.auBlumStefan stefan.blum@brisbaneneurology.com.auBrilot-TurvilleFabienne fabienne.brilot@sydney.edu.au

BrownDavid D.Brown@amr.org.auBruestleAnne Anne.bruestle@anu.edu.au

BundellChristine Chris.Bundell@health.wa.gov.auCampbellIain iain.campbell@sydney.edu.au

ChanFiona fiona120287@gmail.com

CorbettAlastair alastair.corbett@sydney.edu.auDixitAakanksha uqadixit@uq.edu.auFontesAriadna ariadna.fontes@gmail.comFraserClare fraser.clare@gmail.com

FuentesSully Fuentesxiomara@hotmail.comGordonTom t.gordon@flinders.edu.au

GrauGeorges ggrau@med.usyd.edu.au

GreerJudith j.greer@uq.edu.au

GuilleminGilles gilles.guillemin@mq.edu.auGumbertSatya z3220484@student.unsw.edu.au

HiromitsuEna u1041464@anu.edu.auJacksonMichael michael.jackson@flinders.edu.au

JacobsKelly kelly.jacobs@students.mq.edu.auLeeFiona fiona.zheng@sydney.edu.auLopezJoseph jlop3190@uni.sydney.edu.auLovelaceMichael m.lovelace@amr.org.auMatheyEmily emily.mathey@sydney.edu.auMcCombePamela reception@pmccombe.com.au

Moalem-TaylorGila gila@unsw.edu.au

MonifMastura masturamonif@gmail.comMouldJorgen jorgen.mould@merckgroup.com

PhillipsWilliam william.phillips@sydney.edu.au

PillaiSekhar norwestpaedneurology@gmail.comPilliDeepti dpil5654@uni.sydney.edu.auRamanathanSudarshini sudarshini.ramanathan@sydney.edu.au

ReddelStephen swreddel@sydneyneurology.com.auRuitenbergMarc m.ruitenberg@uq.edu.auSardesaiVarda v.sardesai@amr.org.auSiwekKasia kasia.siwek@merckgroup.com

SundaramGayathri g.sundaram@amr.org.au

SwayneAndrew swayneandrew@hotmail.comTanIkLin iltan@hotmail.comTanVanessa vanessa.tan@mq.edu.au

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TeaFiona ftea7693@uni.sydney.edu.auWilsonAlicia alicia.wilson@anu.edu.auWoodberryTonia tonia.woodberry@anu.edu.auZouAlicia alicia_zou3@hotmail.com