Activation-Induced Cytidine Deaminase (AID)-Associated Multigene Signature to Assess Impact of AID in Etiology of Diseases with Inflammatory Component 英文参考文献.docVIP

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Activation-Induced Cytidine Deaminase (AID)-Associated Multigene Signature to Assess Impact of AID in Etiology of Diseases with Inflammatory Component 英文参考文献.doc

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Activation-Induced Cytidine Deaminase (AID)-Associated Multigene Signature to Assess Impact of AID in Etiology of Diseases with Inflammatory Component 英文参考文献

Activation-InducedCytidineDeaminase(AID)-Associated MultigeneSignaturetoAssessImpactofAIDinEtiology ofDiseaseswithInflammatoryComponent DianaMechtcheriakova1*,YurySobanov1,GabrieleHoltappels2,ErikaBajna1,MartinSvoboda1 ,Markus Jaritz3,ClausBachert2,ErikaJensen-Jarolim1 1Department of Pathophysiology and Allergy Research, Center of Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria, 2DepartmentofOtorhinolaryngology,UniversityHospitalGhent,Ghent,Belgium,3ResearchInstituteofMolecularPathology,Vienna,Austria Abstract Activation-inducedcytidinedeaminase(AID)isexpressedinBcellswithingerminalcentersandiscriticallyinvolvedinclass switch recombination and somatic hypermutation of immunoglobulin loci. Functionally active AID can additionally be detectedwithinectopicfollicularstructuresdevelopedatsitesofchronicinflammation.Furthermore,AIDmaytargetnon-Ig genesinB-andnon-B-cellbackground.Therefore,AID-associatedeffectsareofincreasinginterestindiseaseareassuchas allergy, inflammation, autoimmunity, and cancer. Pathway- or disease-relevant multigene signatures have attracted substantialattentionfortherapeutictargetproposal,diagnostictools,andmonitoringoftherapyresponse.Todelineatethe impact of AID in etiology of multifactorial diseases, we designed the AID-associated 25-gene signature. Chronic rhinosinusitis with nasal polyps was used as an inflammation-driven airway disease model; high levels of IgE have been previouslyshowntobepresentwithinpolyptissue.Expressionlevelsof16geneswerefoundtobemodulatedinpolyps includingAID,IgGandIgEmaturetranscriptswhichreflectAIDactivity;clusteringalgorithmrevealedanAID-specificgene signatureforthediseasestatewithnasalpolyp.Complementary,AID-positiveectopiclymphoidstructuresweredetected within polyp tissues by in situ immunostaining. Our data demonstrate the class switch recombination and somatic hypermutationeventslikelytakingplacelocallyintheairwaysandinadditiontothepreviouslyhighlightedmarkersand/or ta