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<p>Several chronic autoimmune diseases are characterized by elevated autoantibody Fab glycosylation. Whether Fab glycans link to disease state or development remains unclear, yet may serve as a marker thereof. Many autoimmune diseases are treated with B cell depletion therapies that particularly result in a decline of autoantibodies. The question arises whether B cell depletion therapy may have an impact on Fab glycosylation. Here, we investigated the longitudinal effects of B cell depletion therapy on Fab glycosylation of total IgG and IgG autoantibodies in rheumatoid arthritis&#xa0;(RA), pemphigus vulgaris&#xa0;(PV), ANCA-associated vasculitis&#xa0;(AAV), and multiple sclerosis&#xa0;(MS). Baseline Fab glycosylation was compared to 6–12 months into therapy by lectin affinity chromatography, determining Fab sialylation as an estimate of Fab glycosylation. We observed a modest decrease in Fab glycosylation of total IgG for RA (median 13.8%[IQR 11.7–16.3] – 9.1%[IQR8-11]) and PV (16.4%[IQR14.9–17.5] – 13.01%[IQR10.8–15.5]) after 6 months, whereas for AAV Fab glycosylation slightly increased (11.6%[IQR7.4–15] – 14.9%[IQR11.4–19.3]), and no changes were found for MS. Autoantibody titers (anti-CCP, anti-PR3, anti-Dsg3) had declined following B cell depletion therapy, yet their elevated Fab glycosylation levels were maintained. Taken together, Fab glycosylation levels of autoantibodies do not decrease upon B cell depletion therapy, thereby retaining their predictive potential as biomarker.</p>

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Elevated Fab glycosylation of autoantibodies maintained during B cell depletion therapy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月28日

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  • Anika M. Valk,
  • Jana Koers,
  • Ninotska I. L. Derksen,
  • Laura Hogenboom,
  • Zoé van Kempen,
  • Joep Killestein,
  • Abraham Rutgers,
  • Peter Heeringa,
  • Barbara Horváth,
  • Taco W. Kuijpers,
  • S. Marieke van Ham,
  • Anja ten Brinke,
  • Diane van der Woude,
  • René E. M. Toes,
  • Nicolaas A. Bos,
  • Theo Rispens,
  • Filip Eftimov,
  • Casper F. M. Franssen,
  • Jaap W. Groothoff,
  • Bart Jacobs,
  • Arnon Kater,
  • Karina de Leeuw,
  • Liesbeth E. M. Oosten,
  • Pieter van Paassen,
  • Uli H. Scherer,
  • Maarten J. Titulaer,
  • Jan Verschuuren,
  • Niek de Vries,
  • Josephine M. I. Vos,
  • J. Hendrik Veelken,
  • Lisa van Baarsen,
  • Eric Eldering,
  • Cecile A. C. M. van Els,
  • Rudi W. Hendriks,
  • Maartje G. Huijbers,
  • Ruth Huizinga,
  • Reina E. Mebius,
  • Jelle de Wit,
  • Jan G. M. C. Damoiseaux,
  • Wayel Abdulahad,
  • Annabel M. Ruiter,
  • Linda van der Weele,
  • Karoline Kielbassa,
  • Mariateresa Coppola,
  • Dorit Verhoeven,
  • Jyaysi Desai,
  • Mirjam van der Burg,
  • Esther M. Vletter,
  • Maaike Braham,
  • Matthias Busch,
  • Carlo Bonasia,
  • Elisabeth Raveling-Eelsing,
  • Niels Verstegen,
  • Casper Marsman,
  • Rocco Sciarillo,
  • Sabrina Pollastro,
  • George Elias,
  • Koos van Dam,
  • Laurent M. Paardekooper,
  • Renée Ysermans,
  • Odilia B. J. Corneth,
  • Anne-Marie Buisman,
  • Rob van Binnendijk,
  • Pauline A. van Schouwenburg,
  • Marvyn Koning,
  • Luuk Wieske,
  • Laura Y. Kummer,
  • Amelie Bos

摘要

Several chronic autoimmune diseases are characterized by elevated autoantibody Fab glycosylation. Whether Fab glycans link to disease state or development remains unclear, yet may serve as a marker thereof. Many autoimmune diseases are treated with B cell depletion therapies that particularly result in a decline of autoantibodies. The question arises whether B cell depletion therapy may have an impact on Fab glycosylation. Here, we investigated the longitudinal effects of B cell depletion therapy on Fab glycosylation of total IgG and IgG autoantibodies in rheumatoid arthritis (RA), pemphigus vulgaris (PV), ANCA-associated vasculitis (AAV), and multiple sclerosis (MS). Baseline Fab glycosylation was compared to 6–12 months into therapy by lectin affinity chromatography, determining Fab sialylation as an estimate of Fab glycosylation. We observed a modest decrease in Fab glycosylation of total IgG for RA (median 13.8%[IQR 11.7–16.3] – 9.1%[IQR8-11]) and PV (16.4%[IQR14.9–17.5] – 13.01%[IQR10.8–15.5]) after 6 months, whereas for AAV Fab glycosylation slightly increased (11.6%[IQR7.4–15] – 14.9%[IQR11.4–19.3]), and no changes were found for MS. Autoantibody titers (anti-CCP, anti-PR3, anti-Dsg3) had declined following B cell depletion therapy, yet their elevated Fab glycosylation levels were maintained. Taken together, Fab glycosylation levels of autoantibodies do not decrease upon B cell depletion therapy, thereby retaining their predictive potential as biomarker.