Differences between Spanish and British patients in the severity of rheumatoid arthritis: comment on the article by Drosos et al.

To the Editor: In their interesting paper, Sfikakis et a1 state " no previous study, to our knowledge, has investigated the in vitro effects of gold compounds on the IL-2/IL-2R [interleukin-2/interleukin-2 receptor] system " (1). This is an oversight, since my colleagues and I have previously shown an in vitro effect of gold sodium thiomalate (GST) on the IL-2/IL-2R system (2). In our experiments, GST inhibited the expression of Tac antigen on phytohemagglutinin-stimulated human T cells. GST also inhibited the prolifera-tive response of T cells to IL-2; this inhibitory effect could be observed even when GST was added after maximum expression of Tac antigens had occurred (2). These observations confirmed those of Wolf and Hall (3), and are complementary to those of Sfikakis and coworkers (1). Gold compounds therefore inhibit lymphocyte responses to IL-2, and the biosynthesis of IL-2 and IL-2R. The work of Sfikakis et a1 shows that this inhibition of biosynthesis occurs, at least in part, at the transcription stage. One criticism of all laboratory work in this area, including ours, is that the concentration of gold to which lymphocytes are exposed (as opposed to the concentration of gold per milliliter of culture medium) is 15-30 fold higher than that which is likely to be found in blood or synovial fluid. This is only one of many variables that must be considered before an in vitro phenomenon could be assumed to occur in the gold-treated patient. 1. Sfikakis PP, Souliotis VL, Panayiotidis PP: Suppression of interleukin-2 and interleukin-2 receptor biosynthesis by gold compounds in in vitro activated human peripheral blood mono-nuclear cells. Inhibition of in vitro proliferation response of cultured T lymphocytes to interleukin-2 by gold sodium thioma-late. Reply To the Editor: We are aware of the article by Harth et a1 in which the inhibitory effect of 20 pg/ml of GST in T cell proliferative responses to exogenous IL-2 is reported (1). This paper confirms the conclusions of a previous report by Wolf and Hall (2), which is cited as reference 6 in our article. Harth et al also reported in their paper, which we inadvertently failed to cite, that the membrane expression of Tac antigen in activated T cells was inhibited by GST; however, this inhibition did not correlate directly with thymidine uptake. Nevertheless, to the best of our knowledge, while these reports include important observations regarding gold's effects on T cell function, suppression of IL-2 …