Adjuvant arthritis is associated with changes in the glycosylation of serum IgG1 and IgG2b

Abstract

SUMMARYThe increased amounts of agalaciosyl IgG (N-linked oligosaccharides terminating with Nacetylglucoseamine (GlcNAe) in the serum of patients with rheumatoid arthritis (RA) and other chronic inflamtnatory diseases have suggested that agalactosyl IgG may be involved in the pathogenesisof RA. We have now evaluated the incidence of agalactosyl IgG in the Lewis rat during the course of adjuvant arthritis (AA). The modificalion in glycosylation of IgG was measured by means of polyclonal and monoclonal anti GlcNAe antibodies as well as by the lectin concanavalin A (Con A). The results show that Lewis rats undergo a change in serum IgG glycosytation during! the course of AA. As in human RA patients, rats with AA lack terminal galacto.se on igG heavy chain oligosaccharides, and the terminal GlcNAe or mannose residues arc thus exposed. The degree of agalactosyl IgG was positively correlated with the incidence of disease, peaked 20 days after disease induction, and the igGgradually reverted to the fully glyeosylated lortn thereafter. The post-arthritic gtycosylation profile was very sitnilar to that characteristic of the naive animal-Purified IgG was shown to contain two IgG subclasses, IgG I and lgG2b. which underwent ehanges in glycosytation. Western blot analysis revealed that IgGl expressed a higher degree oi terminal mannose, whereas IgG 2b expressed a higher degree of terminal GleN.Ac, These lindings raise the question of the possible involvement of agalactosyl igG in itnmtine complex-mediated inflatiimation.

N-glycomic biomarkers of biological aging and longevity: A link with inflammaging

“…Likewise, the presence of IgG-G0 is associated with inflammatory conditions in animal models. For example, arthritis induced by pristane administration in CBA/Igb mice (Rook et al, 1991a), or adjuvant treatment in Lewis rats (Yagev et al, 1993) was accompanied by a rise of IgG-G0. Moreover, in arthritis-prone MLR-lpr/lpr, disease was accompanied by an increase of IgG-G0 (Kuroda et al, 2001a), while in other arthritis prone mice strains arthritis and IgG-G0 rise were induced in parallel by the mere administration of complete Freund adjuvant (Bodman et al, 1994).…”