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Abstract
Studies conducted in rats and mice indicate that passive arthritis can be transferred to naive recipients with anticollagen IgG. The passively transferred disease is less severe and is transient. Rats that recover from passive arthritis are resistant to a second phase of clinical disease when administered either anticollagen IgG or type II collagen. Suppressor T cells appear to be responsible for this resistance.
Passive arthritis induced by anticollagen IgG is a complement dependent lesion. Deposition of IgG on the cartilage and host complement C3 and C5 activation are essential for the induction of passive disease. Inflammatory cells are necessary for the demonstration of passive arthritis; mice deficient in inflammatory cells or defective in this cell population are resistant to passive arthritis.
Monoclonal antibodies reactive to type II collagen or to a renatured TCA fragment can also induce passive arthritis. The disease is subclinical and can be detected only after histological analysis of the joints.