Pemphigus vulgaris is an
autoimmune disease that occurs due to pathogenic
autoantibodies that recognize the following epidermal adhesion
proteins:
desmogleins. Systemic
corticosteroids usually decrease the titers of anti-
desmoglein autoantibodies and improve patients' conditions. Since modifications of
IgG N-glycosylation have been described in some
autoimmune diseases, we hypothesized that changes in the pathogenic activity of
pemphigus IgG could be related to changes in their N-glycosylation profile. The purpose of this study was to assess, longitudinally, the pathogenicity of
pemphigus serum
IgG and their N-glycosylation profile during phases of disease activity and clinical remission. The pathogenic activity of serum
IgG was measured in vitro on immortalized keratinocytes, by immunofluorescence and dissociation assays, and
IgG N-
glycans were analyzed by mass spectrometry. We showed (i) a correlation between
pemphigus clinical activity and the pathogenicity of serum
IgG at baseline and at month 6, while the persistence of the in vitro pathogenic activity of
IgG during its evolution, even in patients in clinical remission, seemed to be predictive of relapse; (ii) that modifications of the N-
glycan structure were altered the in vitro pathogenicity of patients'
autoantibodies; (iii) that the pathogenic properties of
pemphigus IgG did not appear to be related to the disparity in
IgG N-
glycans during the course of
pemphigus.