SUMMARY Using a new solid-phase double-antibody radioimmunoassay we have determined the incidence of serum IgG antibodies to native bovine type I and type II collagens in patients with rheumatoid arthritis (RA), ankylosing spondylitis (AS), and psoriatic arthritis. Raised serum IgG antibody levels to native type I collagen were present in 49 % of patients with RA, 30 % with AS, and none of the patients with psoriatic arthritis. Raised serum IgG antibody levels to native type II collagen were present in 42% of patients with RA, 30 % with AS, and none of the patients with psoriatic arthritis. In rheumatoid arthritis there was a lack of correlation between IgG antibody levels to collagen and the erythrocyte sedimentation rate, IgG rheumatoid factor, and circulating immune complexes measured by the Clq-binding activity. In ankylosing spondylitis IgG antibody levels to native type II collagen were raised only in patients with peripheral joint involvement. The significance of IgG anticollagen antibodies is not certain, but parallels with rheumatoid factor are discussed.

Collagen. Native bovine type RI collagen was extracted from articular cartilage by pepsin solubilisation after previous treatment with 2 M magnesium chloride (Trelsted et al., 1977). Acid-soluble native bovine type I collagen was extracted from fetal calf skin and purified by the method of Jackson and Cleary (1967). Both collagens were lyophilised and stored at -200C until used.The collagen types appeared pure on polyacrylamide gel electrophoresis, and the type II collagen was negative for uronic acid, suggesting that there was no proteoglycan contamination (Bitter and Muir, 1962 (Hudson and Hay, 1976).Adjuvants. All antigens were emulsified in either Freund's complete or incomplete adjuvant (Miles Laboratories Ltd.) in a ratio of 1:1.Injection of rats. Rats were injected intradermally on the back at several sites with 1 ml of emulsion containing 500 ,ug of collagen or rabbit IgG. Booster

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Antibodies to native bovine type II collagen may be important in initiating arthritis in rats immunized with this antigen. The cross-reactivity of these antibodies with native rat type II collagen was higher in rats that developed arthritis than in those that did not. Depletion of serum C3 levels by cobra venom factor delayed the onset of arthritis until C3 levels were returning to normal; therefore, complement may be involved in initiation of the arthritis, and this arthritis may be an example of an immune complex--mediated disease.

An attempt has been made to quantify myocardial lesions produced in the rat by isoprenaline for use as a model to assess possible incremental effects of environmental and dietary factors. This was initially made difficult by variation in the cardiotoxicity of different samples of isoprenaline. Investigation of these samples failed to reveal the basis for the differences. Active preparations have, however, produced profound changes both clinically and pathologically. The earliest light-microscopic changes both clinically and pathologically. The earliest light-microscopic change was loss of fuchsinophilia of fibres in sections stained by the picro-Mallory technique. By 24 hr obvious necrosis, fragmentation and lysis of the fibres had occurred. Treatment of frozen sections to demonstrate succinate dehydrogenase showed early changes in the character of formazan, suggesting the possibility of a transient alteration in the hydrogen transport system. By 48 hr, this is reversed except in those fibres undergoing necrosis where there is a complete loss of formazan. This contrast in staining between normal and necrotic fibres constitutes the basis for quantification which has been carried out by point counting. The results show some differences in the amount of myocardial necrosis between different batches of animals but relatively small differences within individual batches, suggesting that the introduction of additional variants into the system should be capable of producing clear cut results.