Abstract
Although the primary stimulus of inflammation in rheumatoid arthritis (RA) is unknown, data strongly suggest that this inflammation is mediated by activated T-cells, including the prevalence of T-cells in the pannus, the association of the disease with certain MHC class II isotypes (Todd et al, 1988), and the dramatic clinical response to immunosuppressive agents including Cyclosporin A (Dougados et al, 1988; Yocum et al, 1988). Further, several antigen-induced and infectious animal models of arthritis (Collins et al, 1940; Cromartie et al, 1977; Decker et al, 1976; Pearson, 1956; Stuart et al, 1984), as well as chronic Lyme arthritis (Steere et al, 1980) are similar to rheumatoid arthritis, suggesting that unidentified antigens might be responsible for stimulating the T-cells causing this disease. This pathogenic mechanism is also supported by the observation that in several of these animal models, antigen stimulated T-cells and antigen specific T-cell clones derived from animals with arthritis are able to induce a similar illness in naive animals (Holoshitz et al, 1983; Stuart et al, 1984).
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Lafyatis, R., Capron, A. (1994). Expression cloning using antibodies from a patient with rheumatoid arthritis of an autoantigen homologous to the Drosophila splicing regulator, suppressor-of-white-apricot . In: Zouali, M. (eds) Autoimmunity: Experimental Aspects. NATO ASI Series, vol 80. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-78779-9_7
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