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RESEARCH PRODUCT
Molecular Characterization of Virus-induced Autoantibody Responses
Burkhard LudewigBurkhard LudewigÖZlem TüreciPhilippe KrebsPhilippe KrebsJutta TatzelHelen MettersUgur Sahinsubject
DNA ComplementaryTime FactorsautoantibodiesT-LymphocytesvirusesCD40 LigandImmunologyVaccinia virusBiologyLymphocytic choriomeningitisArticleImmunoglobulin GVirusMice03 medical and health sciences0302 clinical medicineAntigenmedicineAnimalsHumansLymphocytic choriomeningitis virusImmunology and AllergyTissue DistributionCD40 AntigensB cellGene Library030304 developmental biologyB-Lymphocytes0303 health sciencesvirus-induced immunopathologyAutoantibodyAntiviral antibodySEREXbiology.organism_classificationmedicine.diseaseVirologytumor immunity3. Good healthMice Inbred C57BLmedicine.anatomical_structureDatabases as TopicVesicular stomatitis virusImmunoglobulin GImmunologybiology.proteinAlgorithms030215 immunologydescription
Here we present a comprehensive molecular mapping of virus-induced autoimmune B cell responses obtained by serological identification of antigens by recombinant expression cloning analysis. Immunoscreening of cDNA expression libraries of various organs (lung, liver, and spleen) using sera from mice infected with cytopathic (vaccinia virus [VV]) or noncytopathic (lymphocytic choriomeningitis virus [LCMV]) viruses revealed a broad specificity of the elicited autoantibody response. Interestingly, the majority of the identified autoantigens have been previously described as autoantigens in humans. We found that induction of virus-induced autoantibodies of the immunoglobulin G class largely depends on the CD40–CD40L-mediated interaction between T and B cells. Furthermore, antibody titers against a number of autoantigens were comparable to the concomitantly induced antiviral antibody response. Comparison of serum reactivity against a selected panel of autoantigens after infection with VV, LCMV, or vesicular stomatitis virus showed that the different virus infections triggered distinct autoantibody responses, suggesting that virus infections may leave specific “autoantibody fingerprints” in the infected host.
year | journal | country | edition | language |
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2004-09-09 | Journal of Experimental Medicine |