Remittive therapy in rheumatoid arthritis: clinical uses and mechanisms of action
Evidence has been reviewed supporting the conclusion that gold compounds, anti-malarials and D-penicillamine have the capacity to function as immunosuppressive drugs. Moreover, the results indicate that each has a unique site of action, specifically inhibiting the function of only one of the populations of cells likely to be involved in chronic immunologically-mediated inflammation. Gold compounds and anti-malarials appear to be active by virtue of their capacity to depress the function of mononuclear phagocytes, while D-penicillamine acts by inhibiting a number of the activities of T lymphocytes. These results imply that the means by which these drugs suppress rheumatoid inflammation are fundamentally different. Thus, while each of these compounds acts as a selective immunosuppressive agent, the target cell inhibited appears to be different. The conclusion that the remission-inducing drugs have different modes of action in RA is supported by the clinical observation that the success rate of therapy with one is comparable regardless of antecedent therapy with another (125, 126).
Evidence has been reviewed supporting the conclusion that gold compounds, anti-malarials and D-penicillamine have the capacity to function as immunosuppressive drugs. Moreover, the results indicate that each has a unique site of action, specifically inhibiting the function of only one of the populations of cells likely to be involved in chronic immunologically-mediated inflammation. Gold compounds and anti-malarials appear to be active by virtue of their capacity to depress the function of mononuclear phagocytes, while D-penicillamine acts by inhibiting a number of the activities of T lymphocytes. These results imply that the means by which these drugs suppress rheumatoid inflammation are fundamentally different. Thus, while each of these compounds acts as a selective immunosuppressive agent, the target cell inhibited appears to be different. The conclusion that the remission-inducing drugs have different modes of action in RA is supported by the clinical observation that the success rate of therapy with one is comparable regardless of antecedent therapy with another (125, 126).
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