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Mader, Simone; Jeganathan, Venkatesh; Arinuma, Yoshiyuki; Fujieda, Yuichiro; Dujmovic, Irena; Drulovic, Jelena; Shimizu, Yuka; Sakuma, Yuko; Stern, Joel N. H.; Aranow, Cynthia; Mackay, Meggan; Yasuda, Shinsuke; Atsumi, Tatsuya; Hirohata, Shunsei; Diamond, Betty

Understanding the Antibody Repertoire in Neuropsychiatric Systemic Lupus Erythematosus and Neuromyelitis Optica Spectrum Disorder : Do They Share Common Targets? : Do They Share Common Targets?

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  • Medientyp: E-Artikel
  • Titel: Understanding the Antibody Repertoire in Neuropsychiatric Systemic Lupus Erythematosus and Neuromyelitis Optica Spectrum Disorder : Do They Share Common Targets? : Do They Share Common Targets?
  • Beteiligte: Mader, Simone; Jeganathan, Venkatesh; Arinuma, Yoshiyuki; Fujieda, Yuichiro; Dujmovic, Irena; Drulovic, Jelena; Shimizu, Yuka; Sakuma, Yuko; Stern, Joel N. H.; Aranow, Cynthia; Mackay, Meggan; Yasuda, Shinsuke; Atsumi, Tatsuya; Hirohata, Shunsei; Diamond, Betty
  • Erschienen: Wiley, 2018
  • Erschienen in: Arthritis & Rheumatology
  • Sprache: Englisch
  • DOI: 10.1002/art.40356
  • ISSN: 2326-5191; 2326-5205
  • Schlagwörter: Immunology ; Rheumatology ; Immunology and Allergy
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:sec><jats:title>Objective</jats:title><jats:p>IgG anti‐<jats:styled-content style="fixed-case">DWEYS</jats:styled-content> antibodies cross‐reactive with <jats:styled-content style="fixed-case">DNA</jats:styled-content> and the <jats:italic>N</jats:italic>‐methyl‐<jats:sc>d</jats:sc>‐aspartate receptor subunits GluN2A and GluN2B are known to be associated with neuropsychiatric systemic lupus erythematosus (<jats:styled-content style="fixed-case">NPSLE</jats:styled-content>). IgG anti‐<jats:styled-content style="fixed-case">DWEYS</jats:styled-content> have not been investigated in demyelinating <jats:styled-content style="fixed-case">NPSLE</jats:styled-content> or in another demyelinating disorder, neuromyelitis optica spectrum disorder (<jats:styled-content style="fixed-case">NMOSD</jats:styled-content>), which is a disease also found mainly in young women and associated with aquaporin 4 (<jats:styled-content style="fixed-case">AQP</jats:styled-content>‐4) or myelin oligodendrocyte glycoprotein (<jats:styled-content style="fixed-case">MOG</jats:styled-content>) antibodies. This study was undertaken to investigate the frequency of all of these brain‐reactive antibodies in patients with <jats:styled-content style="fixed-case">NPSLE</jats:styled-content>, those with demyelinating <jats:styled-content style="fixed-case">NPSLE</jats:styled-content>, and those with <jats:styled-content style="fixed-case">NMOSD</jats:styled-content>.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Serum samples from patients with <jats:styled-content style="fixed-case">NPSLE</jats:styled-content> (n = 108), patients with <jats:styled-content style="fixed-case">SLE</jats:styled-content> without neuropsychiatric manifestations (n = 38), patients with <jats:styled-content style="fixed-case">NMOSD</jats:styled-content> (n = 33), and healthy controls (n = 106) were assessed for the frequency of IgG anti‐brain antibodies as well as IgG antibodies to <jats:styled-content style="fixed-case">AQP</jats:styled-content>‐4, <jats:styled-content style="fixed-case">MOG</jats:styled-content>, GluN2A/GluN2B, and double‐stranded <jats:styled-content style="fixed-case">DNA</jats:styled-content> (ds<jats:styled-content style="fixed-case">DNA</jats:styled-content>).</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Sera were positive for IgG anti–<jats:styled-content style="fixed-case">AQP</jats:styled-content>‐4 antibodies in 27 (82%) of 33 patients with <jats:styled-content style="fixed-case">NMOSD</jats:styled-content> and 3 (27%) of 11 patients with demyelinating <jats:styled-content style="fixed-case">NPSLE</jats:styled-content>, whereas all sera from patients with non‐demyelinating <jats:styled-content style="fixed-case">NPSLE</jats:styled-content>, patients with <jats:styled-content style="fixed-case">SLE</jats:styled-content>, and healthy controls were negative for IgG anti–<jats:styled-content style="fixed-case">AQP</jats:styled-content>‐4. IgG anti‐<jats:styled-content style="fixed-case">MOG</jats:styled-content> were detected at high titers in 3 (50%) of 6 patients with <jats:styled-content style="fixed-case">NMOSD</jats:styled-content> who were negative for IgG anti–<jats:styled-content style="fixed-case">AQP</jats:styled-content>‐4, and at low titers in 2 (18%) of 11 patients with demyelinating <jats:styled-content style="fixed-case">NPSLE</jats:styled-content> and 1 (1%) of 97 patients with non‐demyelinating <jats:styled-content style="fixed-case">NPSLE</jats:styled-content>. IgG antibodies to ds<jats:styled-content style="fixed-case">DNA</jats:styled-content> were present in 11 (33%) of 33 patients with <jats:styled-content style="fixed-case">NMOSD</jats:styled-content>. Only 4 (12%) of 33 patients with <jats:styled-content style="fixed-case">NMOSD</jats:styled-content> were positive for IgG anti‐<jats:styled-content style="fixed-case">DWEYS</jats:styled-content>, compared to 11 (29%) of 38 patients with <jats:styled-content style="fixed-case">SLE</jats:styled-content> and 59 (55%) of 108 patients with <jats:styled-content style="fixed-case">NPSLE</jats:styled-content>. IgG anti‐<jats:styled-content style="fixed-case">DWEYS</jats:styled-content> antibodies were present in 56 (58%) of 97 patients with non‐demyelinating <jats:styled-content style="fixed-case">NPSLE</jats:styled-content> and 3 (27%) of 11 patients with demyelinating <jats:styled-content style="fixed-case">NPSLE</jats:styled-content>. Serum IgG brain‐reactive antibodies were present at a similar frequency in patients with non‐demyelinating <jats:styled-content style="fixed-case">NPSLE</jats:styled-content> (72 [75%] of 96), those with demyelinating <jats:styled-content style="fixed-case">NPSLE</jats:styled-content> (9 [82%] of 11), and those with <jats:styled-content style="fixed-case">SLE</jats:styled-content> (32 [84%] of 38), but were less frequent in patients with <jats:styled-content style="fixed-case">NMOSD</jats:styled-content> (20 [61%] of 33).</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Patients with demyelinating <jats:styled-content style="fixed-case">NPSLE</jats:styled-content> should be tested for IgG antibodies to <jats:styled-content style="fixed-case">AQP</jats:styled-content>‐4, <jats:styled-content style="fixed-case">MOG</jats:styled-content>, and <jats:styled-content style="fixed-case">DWEYS</jats:styled-content>. IgG anti–<jats:styled-content style="fixed-case">AQP</jats:styled-content>‐4 can be considered diagnostic for <jats:styled-content style="fixed-case">NMOSD</jats:styled-content>, whereas none of these antibodies appear to be diagnostic for demyelinating <jats:styled-content style="fixed-case">NPSLE</jats:styled-content>. Moreover, IgG anti‐ds<jats:styled-content style="fixed-case">DNA</jats:styled-content> are present in patients with <jats:styled-content style="fixed-case">NMOSD</jats:styled-content> but are not cross‐reactive with IgG anti‐<jats:styled-content style="fixed-case">DWEYS</jats:styled-content>, indicating that the antigenic stimulus and mechanisms of tissue damage are potentially different between demyelinating <jats:styled-content style="fixed-case">NPSLE</jats:styled-content> and <jats:styled-content style="fixed-case">NMOSD</jats:styled-content>.</jats:p></jats:sec>
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