Rheumatoid arthritis pathogenesis pdf, [PDF] Etanercept-induced subacute thyroiditis | Semantic Scholar

DOI: B cell depleting therapies may result in a transient immunosuppression, increasing the risk of infections. Our aim was to develop a new therapeutic approach to selectively deplete the ACPA producing autoreactive B cells.

Methods: To target B cells synthetic citrullinated peptide derived from the beta chain of fibrin, beta Cit 60,72,74 beta Citthe predominant epitope recognized by ACPA was used. To trigger CDC both the targeting peptide and the complement activating peptide were covalently coupled in multiple copies to the surface of poly DL-lactic-co-glycolic acid nanoparticles NPs.

CDC was tested after dead cell staining by flow cytometry.

Results: The beta Cit peptide was selectively recognized by a small subset of Rheumatoid arthritis pathogenesis pdf cells from RA patients having high level of peptide specific serum antibody, suggesting that the peptide can target diseased B cells. The modified gp peptide covalently coupled to NPs induced the formation of the complement membrane attack complex, C5b-9 in human serum. We show here for the first time that bifunctional NPs coupled to multiple copies of both the targeting peptide and the complement activating effector peptide on their surface significantly reduce beta Cit peptide specific ex vivo ACPA production, by inducing complement dependent lysis of the citrullinated peptide specific B rheumatoid arthritis pathogenesis pdf of seropositive RA patients.

Conclusions: Bifunctional NPs covalently coupled to autoantigen epitope peptide and to a lytic peptide activating complement may specifically target and deplete the peptide specific autoreactive B-cells.