Affinity-purified rabbit anticollagen IgG failed to transfer arthritis to rats when it was injected intravenously. Immunofluorescence examination of the joints of the hind paws of recipient rats showed the deposition of rabbit IgG on the articular surfaces; however, C4 or C3 deposition was not detected. In recipient rats injected intravenously with equivalent amounts of rat anticollagen IgG, arthritis occurred within 48 hr; IgG, C4, and C3 could be detected on the articular surface. Rats given Type II collagen intravenously accumulated inflammatory cells in the pleural cavity in response to a subsequent challenge with intrapleural rat anticollagen IgG; with rabbit anticollagen IgG significantly fewer cells accumulated. Rabbit anticollagen IgG did not promote the lysis of Type II collagen coated sheep red blood cells that were incubated with rat serum. In parallel control experiments, lysis of cells occurred when rat serum was added to either sheep cells coated with Type II collagen and incubated with rat anticollagen IgG or sheep cells coated with bovine serum albumin and incubated with rabbit anti-bovine serum albumin. These observations suggest that the failure of rabbit anticollagen IgG to transfer arthritis to rats is, at least in part, due to its inability to activate rat complement.
ASJC Scopus subject areas
- Immunology and Allergy
- Pathology and Forensic Medicine