IgG N-Glycosylation from Patients with Pemphigus Treated with Rituximab - Normandie Université Access content directly
Journal Articles Biomedicines Year : 2022

IgG N-Glycosylation from Patients with Pemphigus Treated with Rituximab


Pemphigus is a life-threatening auto-immune blistering disease of the skin and mucous membrane that is caused by the production of auto-antibodies (auto-Abs) directed against adhesion proteins: desmoglein 1 and 3. We demonstrated in the "Ritux3" trial, the high efficacy of rituximab, an anti-CD20 recombinant monoclonal antibody, as the first-line treatment for pemphigus. However, 25% of patients relapsed during the six-month period after rituximab treatment. These early relapses were associated with a lower decrease in anti-desmoglein auto-Abs after the initial cycle of rituximab. The N-glycosylation of immunoglobulin-G (IgG) can affect their affinity for Fc receptors and their serum half-life. We hypothesized that the extended half-life of Abs could be related to modifications of IgG N-glycans. The IgG N-glycome from pemphigus patients and its evolution under rituximab treatment were analyzed. Pemphigus patients presented a different IgG N-glycome than healthy donors, with less galactosylated, sialylated N-glycans, as well as a lower level of N-glycans bearing an additional N-acetylglucosamine. IgG N-glycome from patients who achieved clinical remission was not different to the one observed at baseline. Moreover, our study did not identify the N-glycans profile as discriminating between relapsing and non-relapsing patients. We report that pemphigus patients present a specific IgG N-glycome. The changes observed in these patients could be a biomarker of autoimmunity susceptibility rather than a sign of inflammation.
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hal-03738179 , version 1 (25-07-2022)



Guillaume Font, Marie-Laure Walet-Balieu, Marie Petit, Carole Burel, Maud Maho-Vaillant, et al.. IgG N-Glycosylation from Patients with Pemphigus Treated with Rituximab. Biomedicines, 2022, 10 (8), pp.1774. ⟨10.3390/biomedicines10081774⟩. ⟨hal-03738179⟩
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