Abstract
It cannot be denied that the rheumatic joint is the site of an intense immunological activity1. The joint is heavily populated by lymphocytes, macrophages and polymorphonuclear cells2. B-cells are hyperactive and produce large amounts of antibodies, some of which are directed against the patient’s own immunoglobulins3–5. There is increased complement consumption6 and formation of immune complexes2,7. But the most outstanding clinical feature of rheumatoid arthritis is the formation and persistence of chronic granulomata within the joints and other tissues8. The predominant infiltrating lymphocyte is the T-cell9. This T-cell seems to be functionally active since lymphokines are produced in the rheumatic joint10 and since patients with rheumatoid arthritis possess cell-mediated immunity to autologous IgG and to antigens present in the rheumatoid synovium11,12.
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Symoens, J. (1977). The rationale of using levamisole in the treatment of rheumatoid arthritis. In: Willoughby, D.A., Giroud, J.P., Velo, G.P. (eds) Perspectives in Inflammation. Future Trends in Inflammation, vol 3. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-7185-4_1
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