FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2410176384> ?p ?o ?g. }

• W2410176384 abstract "Background Antibody Fab fragments (Fabs) maintain the ability to bind to specific antigens but lack the binding site for complement as well as the site for binding to receptors on immune and inflammatory cells that play a critical role in autoimmune diseases including collagen-induced arthritis (CIA) in mice. Therefore, CIA might be regulated by type II collagen (CII)-specific antibody Fabs. Objectives The present study was performed to investigate the effect of Fabs of arthritogenic CII-specific IgG2b (C2B-9 and C2B-14) monoclonal antibodies (mAb) on CIA and to define the mechanism underlying the suppression of the autoimmune joint inflammation by the Fabs. Methods To induce CIA, DBA/1J mice were immunized by subcutaneous injections of CII plus CFA into the base of the tail on days 0 and 21. Hybridomas producing C2B-9 and C2B-14 were established by fusing anti-CII antibody-producing spleen cells and myeloma cells. C2B-9 and C2B-14 Fabs were prepared by the digestion of the CII-specific mAbs with papain and injected i.p. on days -1 and 3. The effect of the Fabs on CIA was evaluated clinically, serologically, and histologically. Results Treatment with C2B-9 or C2B-14 Fabs alone failed to suppress CIA. In contrast, the combination of C2B-9 and C2B-14 Fabs significantly suppressed both the incidence and the severity of CIA. The suppression of CIA by the Fabs was associated with a decrease in CII-specific IgG in serum. Histologically, proliferation of synovium, infiltration of inflammatory cells including mononuclear cells, and destruction of cartilage and subchondral bone were diminished in C2B-9 and C2B-14 Fab-treated animals. In vitro studies revealed that the capture of CII by O2B-9 or O2B-14 Fabs prevented the subsequent binding of intact anti-CII polyclonal antibodies to the captured CII. Conclusions These results suggest that autoimmune inflammatory diseases such as rheumatoid arthritis might be specifically regulated by pathogenic mAb Fabs via the interference with autoantigen-intact autoantibody interaction by the fragments, resulting in the suppression of complement and immune/inflammatory cell activation. References Yoshino, S., et al., Br. J. Pharmacol., 161:1351-1360, 2010. Koobkokkruad, T., and Yoshino, S., et al., J. Inflamm., 8:31-37,2011. Yoshino, S., et al., Immunol., 141:617-627, 2014. Disclosure of Interest None declared" @default.
• W2410176384 created "2016-06-24" @default.
• W2410176384 creator A5085953868 @default.
• W2410176384 date "2015-06-01" @default.
• W2410176384 modified "2023-09-27" @default.
• W2410176384 title "AB0142 Suppression of Collagen-Induced Arthritis in Mice by Fab Fragments of Arthritogenic Anti-Type II Collagen Monoclonal Antibodies" @default.
• W2410176384 doi "https://doi.org/10.1136/annrheumdis-2015-eular.2017" @default.
• W2410176384 hasPublicationYear "2015" @default.
• W2410176384 type Work @default.
• W2410176384 sameAs 2410176384 @default.
• W2410176384 citedByCount "0" @default.
• W2410176384 crossrefType "journal-article" @default.
• W2410176384 hasAuthorship W2410176384A5085953868 @default.
• W2410176384 hasConcept C147483822 @default.
• W2410176384 hasConcept C153911025 @default.
• W2410176384 hasConcept C159654299 @default.
• W2410176384 hasConcept C203014093 @default.
• W2410176384 hasConcept C2776914184 @default.
• W2410176384 hasConcept C2777077863 @default.
• W2410176384 hasConcept C2780931953 @default.
• W2410176384 hasConcept C542903549 @default.
• W2410176384 hasConcept C71924100 @default.
• W2410176384 hasConcept C86803240 @default.
• W2410176384 hasConcept C8891405 @default.
• W2410176384 hasConceptScore W2410176384C147483822 @default.
• W2410176384 hasConceptScore W2410176384C153911025 @default.
• W2410176384 hasConceptScore W2410176384C159654299 @default.
• W2410176384 hasConceptScore W2410176384C203014093 @default.
• W2410176384 hasConceptScore W2410176384C2776914184 @default.
• W2410176384 hasConceptScore W2410176384C2777077863 @default.
• W2410176384 hasConceptScore W2410176384C2780931953 @default.
• W2410176384 hasConceptScore W2410176384C542903549 @default.
• W2410176384 hasConceptScore W2410176384C71924100 @default.
• W2410176384 hasConceptScore W2410176384C86803240 @default.
• W2410176384 hasConceptScore W2410176384C8891405 @default.
• W2410176384 hasLocation W24101763841 @default.
• W2410176384 hasOpenAccess W2410176384 @default.
• W2410176384 hasPrimaryLocation W24101763841 @default.
• W2410176384 hasRelatedWork W1501734887 @default.
• W2410176384 hasRelatedWork W1510409387 @default.
• W2410176384 hasRelatedWork W1511061280 @default.
• W2410176384 hasRelatedWork W1589149139 @default.
• W2410176384 hasRelatedWork W1918965609 @default.
• W2410176384 hasRelatedWork W2014494635 @default.
• W2410176384 hasRelatedWork W2019178946 @default.
• W2410176384 hasRelatedWork W2024303898 @default.
• W2410176384 hasRelatedWork W2040619664 @default.
• W2410176384 hasRelatedWork W2048283288 @default.
• W2410176384 hasRelatedWork W2065824890 @default.
• W2410176384 hasRelatedWork W2075355645 @default.
• W2410176384 hasRelatedWork W2091490997 @default.
• W2410176384 hasRelatedWork W2119663838 @default.
• W2410176384 hasRelatedWork W2143896178 @default.
• W2410176384 hasRelatedWork W2160359647 @default.
• W2410176384 hasRelatedWork W2327229699 @default.
• W2410176384 hasRelatedWork W2412312499 @default.
• W2410176384 hasRelatedWork W3143631112 @default.
• W2410176384 hasRelatedWork W3086256600 @default.
• W2410176384 isParatext "false" @default.
• W2410176384 isRetracted "false" @default.
• W2410176384 magId "2410176384" @default.
• W2410176384 workType "article" @default.