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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 <i>N-</i>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 <i>N-</i>glycans. The IgG <i>N-</i>glycome from pemphigus patients and its evolution under rituximab treatment were analyzed. Pemphigus patients presented a different IgG <i>N-</i>glycome than healthy donors, with less galactosylated, sialylated <i>N-</i>glycans, as well as a lower level of <i>N-</i>glycans bearing an additional <i>N-</i>acetylglucosamine. IgG <i>N-</i>glycome from patients who achieved clinical remission was not different to the one observed at baseline. Moreover, our study did not identify the <i>N-</i>glycans profile as discriminating between relapsing and non-relapsing patients. We report that pemphigus patients present a specific IgG <i>N-</i>glycome. The changes observed in these patients could be a biomarker of autoimmunity susceptibility rather than a sign of inflammation.