Abstract
Prospective and retrospective analysis of data obtained on 119 patients with rheumatoid arthritis suggested a relationship between clinical response induced by gold salts or D-penicillamine and decreased in vitro antibody synthesis by peripheral blood mononuclear cells. A subgroup of 21 patients with inactive disease receiving these drugs was found to have decreased pokeweed mitogen-induced in vitro synthesis of IgM and IgM rheumatoid factor. Detailed analysis of the cellular mechanisms responsible for this decreased responsiveness demonstrated markedly decreased B cell function. Patients treated with D-penicillamine also had altered T cell helper function manifested by incomplete reconstitution of the normal IgM response, while patients treated with gold salts had normal T cell function. Monocytes appeared not to have a major role in the decreased in vitro responsiveness. The results suggest that, in patients who respond to gold salts or D-penicillamine, antibody synthesis by circulating B cells is profoundly decreased, probably due to an indirect effect of these disease-modifying agents.