Passive transfer studies with type II collagen antibody in B10.D2/old and new line and C57Bl/6 normal and beige (Chediak-Higashi) strains: evidence of important roles for C5 and multiple inflammatory cell types in the development of erosive arthritis.
C5-normal B10.D2/new line mice were susceptible to passively transferred arthritis from purified type II collagen antibody, and in vitro studies demonstrated that, when bound to cartilage, this antibody readily activated complement C5 to C5a. C5-deficient B10.D2/old line mice failed to develop passively transferred arthritis, despite the deposition of antibody and C3 along the cartilage surface. C57Bl/6 mice were susceptible to passively transferred arthritis, which was characterized in histopathologic studies as an erosive synovitis involving multiple inflammatory cell types. In contrast, neither clinical nor histologic evidence of arthritis was observed in C57Bl/6 mice with the beige mutation (Chediak-Higashi syndrome).
D000818:Animals; D001168:Arthritis / Q000276:immunology* / Q000473:pathology; D002358:Cartilage, Articular / Q000276:immunology; D003094:Collagen / Q000276:immunology*; D003167:Complement Activation; D003182:Complement C5 / Q000172:deficiency / Q000502:physiology*; D005260:Female; D007116:Immunization, Passive; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D008817:Mice, Mutant Strains; D008853:Microscopy; D008854:Microscopy, Electron; D051381:Rats
D003182:Complement C5; D003094:Collagen