Reemergence of pathogenic, autoantibody-producing B cell clones in myasthenia gravis following B cell depletion therapy
Fichtner ML, Hoehn KB, Ford EE, Mane-Damas M, Oh S, Waters P, Payne AS, Smith ML, Watson CT, Losen M, Martinez-Martinez P, Nowak RJ, Kleinstein SH, O’Connor K. Reemergence of pathogenic, autoantibody-producing B cell clones in myasthenia gravis following B cell depletion therapy. Acta Neuropathologica Communications 2022, 10: 154. PMID: 36307868, PMCID: PMC9617453, DOI: 10.1186/s40478-022-01454-0.Peer-Reviewed Original ResearchConceptsB cell depletion therapyB cell clonesMuSK-MG patientsMyasthenia gravisB cellsMG patientsDepletion therapyCell clonesAutoantibody-producing B cellsMuscle-specific tyrosine kinaseComplete stable remissionB cell receptor repertoireCell receptor repertoireValuable candidate biomarkersB cell receptorMG relapseClinical relapseStable remissionDisease relapseAutoimmune disordersRelapsePatientsAcetylcholine receptorsCandidate biomarkersReceptor repertoireMyasthenia gravis complement activity is independent of autoantibody titer and disease severity
Fichtner ML, Hoarty MD, Vadysirisack DD, Munro-Sheldon B, Nowak RJ, O’Connor K. Myasthenia gravis complement activity is independent of autoantibody titer and disease severity. PLOS ONE 2022, 17: e0264489. PMID: 35290370, PMCID: PMC8923450, DOI: 10.1371/journal.pone.0264489.Peer-Reviewed Original ResearchConceptsAutoantibody titersComplement activityDisease activityMyasthenia gravisComplement pathwayAcetylcholine receptor autoantibodiesAutoimmune myasthenia gravisSecondary complement deficiencyClassical complement pathwayAChR autoantibodiesReceptor autoantibodiesClinical statusAutoimmune diseasesHealthy controlsComplement deficiencyPatients associatesStudy subjectsCandidate biomarkersDisease statusDisease severitySignificant associationDisease pathologyTitersAutoantibodiesPatients