Differentiated pattern of complement system activation between MOG-IgG-associated disease and AQP4-IgG-positive neuromyelitis optica spectrum disorder
DC Field | Value | Language |
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dc.contributor.author | Cho, Eun Bin | - |
dc.contributor.author | Min, Ju-Hong | - |
dc.contributor.author | Waters, Patrick | - |
dc.contributor.author | Jeon, Miyoung | - |
dc.contributor.author | Ju, Eun-Seon | - |
dc.contributor.author | Kim, Ho Jin | - |
dc.contributor.author | Kim, Su-Hyun | - |
dc.contributor.author | Shin, Ha Young | - |
dc.contributor.author | Kang, Sa-Yoon | - |
dc.contributor.author | Lim, Young-Min | - |
dc.contributor.author | Oh, Sun-Young | - |
dc.contributor.author | Lee, Hye Lim | - |
dc.contributor.author | Sohn, Eunhee | - |
dc.contributor.author | Lee, Sang-Soo | - |
dc.contributor.author | Oh, Jeeyoung | - |
dc.contributor.author | Kim, Sunyoung | - |
dc.contributor.author | Huh, So-Young | - |
dc.contributor.author | Cho, Joong-Yang | - |
dc.contributor.author | Seok, Jin Myoung | - |
dc.contributor.author | Kim, Byung-Jo | - |
dc.contributor.author | Kim, Byoung Joon | - |
dc.date.accessioned | 2024-06-12T02:30:24Z | - |
dc.date.available | 2024-06-12T02:30:24Z | - |
dc.date.issued | 2024-03 | - |
dc.identifier.issn | 1664-3224 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/26346 | - |
dc.description.abstract | Background Myelin oligodendrocyte glycoprotein antibody (MOG) immunoglobulin G (IgG)-associated disease (MOGAD) has clinical and pathophysiological features that are similar to but distinct from those of aquaporin-4 antibody (AQP4-IgG)-positive neuromyelitis optica spectrum disorders (AQP4-NMOSD). MOG-IgG and AQP4-IgG, mostly of the IgG1 subtype, can both activate the complement system. Therefore, we investigated whether the levels of serum complement components, regulators, and activation products differ between MOGAD and AQP4-NMOSD, and if complement analytes can be utilized to differentiate between these diseases. Methods The sera of patients with MOGAD (from during an attack and remission; N=19 and N=9, respectively) and AQP4-NMOSD (N=35 and N=17), and healthy controls (N=38) were analyzed for C1q-binding circulating immune complex (CIC-C1q), C1 inhibitor (C1-INH), factor H (FH), C3, iC3b, and soluble terminal complement complex (sC5b-9). Results In attack samples, the levels of C1-INH, FH, and iC3b were higher in the MOGAD group than in the NMOSD group (all, p<0.001), while the level of sC5b-9 was increased only in the NMOSD group. In MOGAD, there were no differences in the concentrations of complement analytes based on disease status. However, within AQP4-NMOSD, remission samples indicated a higher C1-INH level than attack samples (p=0.003). Notably, AQP4-NMOSD patients on medications during attack showed lower levels of iC3b (p<0.001) and higher levels of C3 (p=0.008), C1-INH (p=0.004), and sC5b-9 (p<0.001) compared to those not on medication. Among patients not on medication at the time of attack sampling, serum MOG-IgG cell-based assay (CBA) score had a positive correlation with iC3b and C1-INH levels (rho=0.764 and p=0.010, and rho=0.629 and p=0.049, respectively), and AQP4-IgG CBA score had a positive correlation with C1-INH level (rho=0.836, p=0.003). Conclusions This study indicates a higher prominence of complement pathway activation and subsequent C3 degradation in MOGAD compared to AQP4-NMOSD. On the other hand, the production of terminal complement complexes (TCC) was found to be more substantial in AQP4-NMOSD than in MOGAD. These findings suggest a strong regulation of the complement system, implying its potential involvement in the pathogenesis of MOGAD through mechanisms that extend beyond TCC formation. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | FRONTIERS MEDIA SA | - |
dc.title | Differentiated pattern of complement system activation between MOG-IgG-associated disease and AQP4-IgG-positive neuromyelitis optica spectrum disorder | - |
dc.type | Article | - |
dc.publisher.location | 스위스 | - |
dc.identifier.doi | 10.3389/fimmu.2024.1320094 | - |
dc.identifier.scopusid | 2-s2.0-85189549927 | - |
dc.identifier.wosid | 001196015600001 | - |
dc.identifier.bibliographicCitation | FRONTIERS IN IMMUNOLOGY, v.15 | - |
dc.citation.title | FRONTIERS IN IMMUNOLOGY | - |
dc.citation.volume | 15 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.subject.keywordPlus | GLYCOPROTEIN | - |
dc.subject.keywordAuthor | myelin oligodendrocyte glycoprotein | - |
dc.subject.keywordAuthor | neuromyelitis optica spectrum disorder | - |
dc.subject.keywordAuthor | complement | - |
dc.subject.keywordAuthor | terminal complement complex (sC5b-9) | - |
dc.subject.keywordAuthor | classical complement cascade | - |
dc.subject.keywordAuthor | alternative complement activity | - |
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