SWR mice are resistant to collagen-induced arthritis but produce potentially arthritogenic antibodies.

SWR mice are resistant to collagen-induced arthritis but produce antibodies to type II collagen. To determine if these antibodies have arthritogenic potential, serum from collagen-immunized mice was concentrated and passively transferred to DBA/1 mice. The recipients developed severe arthritis within 72 hours. To evaluate the role of complement, SWR mice were bred with congenic inbred B10.D2/oSn (complement deficient) and B10.D2/nSn (complement normal) mice. Collagen-immunized (SWR x B10.D2/nSn)F1 mice had high levels of C5 and were susceptible to arthritis, while (SWR x B10.D2/oSn)F1 mice were deficient in C5 and were resistant to arthritis.

Induction of erosive arthritis in mice after passive transfer of anti-type II collagen antibodies.

The passive transfer of concentrated immunoglobulins or affinity-purified anti-collagen antibodies from sera of mice with type II collagen-induced arthritis can induce erosive arthritis in recipient animals. In both cases, the incidence of arthritis was over 60% and the inflammation persisted for at least two weeks. Radiography revealed bone destruction and apposition of a newly formed material while histologic examination showed cartilage and bone degradation, accompanied with synovitis and periarthritis. Inflammatory infiltrates were composed of polymorphonuclear leucocytes and lymphocytes, and were associated with a proliferation of connective tissue cells.

Delayed type hypersensitivity (DTH) to type II collagen (CII) in DBA-1 mice.

Sensitization of DBA-1 mice with Type II collagen (CII) in complete Freund's adjuvant can cause polyarthritis. A possible link between CII-induced arthritis and delayed type hypersensitivity (DTH) has been suggested, so we decided to investigate the susceptibility of DBA-1 mice to CII induced DTH reactions. The mice were primed with a dose of 10 micrograms CII i.p. 4 days before challenging with 40 micrograms CII in the ear. Swelling was measured 48 h later and was found to be reproducible. Responsiveness to CII could be transferred with whole spleen cell populations from primed animals or with enriched spleen T cells, thus confirming the cellular nature of the reaction. Lymph node cells from CII/CFA footpad immunized animals were restimulated with CII in vitro. These cells were able to passively transfer DTH sensitivity in vivo and exhibited specificity for this antigen in vitro in proliferation assays.