“…Percy et al,27 using their arbitrary normal/abnormal classification of lymphocyte transformation, showed an association between improvement in disease and improvement in lymphocyte response. In a similar manner on our arbitrary definition of a response to gold therapy there is a significant association between a normal con-A concentration at [15][16][17][18][19][20][21][22][23][24] weeks and a favourable response to gold therapy (X2 = 10-4, P = 0-01 with Yates's correction for small numbers). However, the numbers are small (4 out of 5 nonresponders outside the normal range after treatment) and the association did not hold for PHA and PWM.…”
Section: Discussionmentioning
confidence: 85%
“…The improvement over pretreatment values was significant for con-A and PWM when measured as area and for con-A when response at optimal concentration is considered. Thus, in this n=14 [15][16][17][18][19][20][21][22][23][24] group of patients there was an overall trend towards improvement of lymphocyte mitogen responsiveness during gold treatment. This contrasts with the suppressive effects of gold salts added to lymphocyte cultures in vitro.…”
Section: Discussionmentioning
confidence: 93%
“…Measel'7 showed an increased antibody response to sheep red blood cells and type III pneumococcal polysaccharide when gold was injected at the same time as the antigen. Scheiffarth et al 18 showed a similar effect in mice when gold was given at the same time as antigen but a decrease in antibody response when gold was given 12 weeks prior to the antigen. Persellin et al'9 found that gold did not inhibit antibody response to typhoid and paratyphoid vaccine or bovine serum albumin in rabbits.…”
mentioning
confidence: 90%
“…After treatment the difference from normal persons remained significant with PWM. However, when only these optimal concentrations are considered, the improvement in lymphocyte responsiveness over pretreatment levels after [15][16][17][18][19][20][21][22][23][24] weeks of gold treatment is significant only with con-A.…”
SUMMARY The mitogenic response of peripheral blood lymphocytes from21 patients with rheumatoid arthritis to concanavalin-A (con-A), phytohaemagglutinin (PHA), and pokeweed mitogen (PWM) was significantly lower than in 30 normal subjects. After 15-24 weeks' treatment with sodium aurothiomalate (GST) the response to these mitogens rose to within the normal range. Improvement over pretreatment values was significant for con-A and PWM measured as area under the dose response curve but only for con-A if response at optimal mitogen concentration is the sole criterion. The improvement in PHA response was not significant with either method of measurement. There was an improvement in disease activity by 15-24 weeks as measured by a fall in serum C-reactive protein (CRP), IgM rheumatoid factor (RF), Clq binding activity (C1qBA), and Ritchie articular index. Con-A lymphocyte responsiveness was inversely related to serum CRP levels, but measurements of disease activity were otherwise unrelated to lymphocyte mitogen responsiveness. The observed improvement in peripheral blood lymphocyte responsiveness during gold treatment contrasts with the suppressive effect of gold in vitro. We suggest that the improvement in lymphocyte function is due to the lessening of rheumatoid disease activity during gold treatment, and that the low serum gold levels in our patients were insufficient to mask this effect. Sera from some of our patients were capable of suppressing the function of normal lymphocyfes, and this was less apparent after treatment. The suppressive effect of sera correlated with ClqBA. Suppressive factors in serum, including possibly immune complexes, may be one factor leading to suppression of lymphocyte function during rheumatoid arthritis. Such an inverse relationship between humoral and cellular immune mechanisms might influence the clinical expression of rheumatoid arthritis.Gold salts have been shown in controlled trials to be most apparent with gold concentrations of 10-100 effective in the treatment of rheumatoid arthritis.1-3 ,tg/ml and has been shown to be due to an effect on However, the means by which gold inhibits inflam-monocytes. Rosenberg and Lipsky1" have also mation in rheumatoid arthritis is unknown, although shown that gold can inhibit pokeweed mitogen a wide variety of mechanisms have been investi-induced immunoglobulin production by human gated.4 As immunological processes, and especially lymphocytes. Gold has an inhibitory effect on the the function of lymphocytes,5 are thought to be mixed leucocyte reaction7 91012 and cell-mediated important in the pathogenesis of the disease, the cytotoxicity9 12 13 when present at the initiation of effects of gold on immune mechanisms have been culture.9 13 Thus, there is evidence from in-vitro studied.experiments with human peripheral blood mono-A number of studies6-10 have shown that gold nuclear cells that gold inhibits several lymphocyte present at the initiation of lymphocyte cultures in functions, possibly due to its effect on monocytes. vitro suppresses lymph...
“…Percy et al,27 using their arbitrary normal/abnormal classification of lymphocyte transformation, showed an association between improvement in disease and improvement in lymphocyte response. In a similar manner on our arbitrary definition of a response to gold therapy there is a significant association between a normal con-A concentration at [15][16][17][18][19][20][21][22][23][24] weeks and a favourable response to gold therapy (X2 = 10-4, P = 0-01 with Yates's correction for small numbers). However, the numbers are small (4 out of 5 nonresponders outside the normal range after treatment) and the association did not hold for PHA and PWM.…”
Section: Discussionmentioning
confidence: 85%
“…The improvement over pretreatment values was significant for con-A and PWM when measured as area and for con-A when response at optimal concentration is considered. Thus, in this n=14 [15][16][17][18][19][20][21][22][23][24] group of patients there was an overall trend towards improvement of lymphocyte mitogen responsiveness during gold treatment. This contrasts with the suppressive effects of gold salts added to lymphocyte cultures in vitro.…”
Section: Discussionmentioning
confidence: 93%
“…Measel'7 showed an increased antibody response to sheep red blood cells and type III pneumococcal polysaccharide when gold was injected at the same time as the antigen. Scheiffarth et al 18 showed a similar effect in mice when gold was given at the same time as antigen but a decrease in antibody response when gold was given 12 weeks prior to the antigen. Persellin et al'9 found that gold did not inhibit antibody response to typhoid and paratyphoid vaccine or bovine serum albumin in rabbits.…”
mentioning
confidence: 90%
“…After treatment the difference from normal persons remained significant with PWM. However, when only these optimal concentrations are considered, the improvement in lymphocyte responsiveness over pretreatment levels after [15][16][17][18][19][20][21][22][23][24] weeks of gold treatment is significant only with con-A.…”
SUMMARY The mitogenic response of peripheral blood lymphocytes from21 patients with rheumatoid arthritis to concanavalin-A (con-A), phytohaemagglutinin (PHA), and pokeweed mitogen (PWM) was significantly lower than in 30 normal subjects. After 15-24 weeks' treatment with sodium aurothiomalate (GST) the response to these mitogens rose to within the normal range. Improvement over pretreatment values was significant for con-A and PWM measured as area under the dose response curve but only for con-A if response at optimal mitogen concentration is the sole criterion. The improvement in PHA response was not significant with either method of measurement. There was an improvement in disease activity by 15-24 weeks as measured by a fall in serum C-reactive protein (CRP), IgM rheumatoid factor (RF), Clq binding activity (C1qBA), and Ritchie articular index. Con-A lymphocyte responsiveness was inversely related to serum CRP levels, but measurements of disease activity were otherwise unrelated to lymphocyte mitogen responsiveness. The observed improvement in peripheral blood lymphocyte responsiveness during gold treatment contrasts with the suppressive effect of gold in vitro. We suggest that the improvement in lymphocyte function is due to the lessening of rheumatoid disease activity during gold treatment, and that the low serum gold levels in our patients were insufficient to mask this effect. Sera from some of our patients were capable of suppressing the function of normal lymphocyfes, and this was less apparent after treatment. The suppressive effect of sera correlated with ClqBA. Suppressive factors in serum, including possibly immune complexes, may be one factor leading to suppression of lymphocyte function during rheumatoid arthritis. Such an inverse relationship between humoral and cellular immune mechanisms might influence the clinical expression of rheumatoid arthritis.Gold salts have been shown in controlled trials to be most apparent with gold concentrations of 10-100 effective in the treatment of rheumatoid arthritis.1-3 ,tg/ml and has been shown to be due to an effect on However, the means by which gold inhibits inflam-monocytes. Rosenberg and Lipsky1" have also mation in rheumatoid arthritis is unknown, although shown that gold can inhibit pokeweed mitogen a wide variety of mechanisms have been investi-induced immunoglobulin production by human gated.4 As immunological processes, and especially lymphocytes. Gold has an inhibitory effect on the the function of lymphocytes,5 are thought to be mixed leucocyte reaction7 91012 and cell-mediated important in the pathogenesis of the disease, the cytotoxicity9 12 13 when present at the initiation of effects of gold on immune mechanisms have been culture.9 13 Thus, there is evidence from in-vitro studied.experiments with human peripheral blood mono-A number of studies6-10 have shown that gold nuclear cells that gold inhibits several lymphocyte present at the initiation of lymphocyte cultures in functions, possibly due to its effect on monocytes. vitro suppresses lymph...
“…1963; Jessop et al 1973), an effect consistent with the inhibition of cell immigration observed with different dosing regimes. There are, however, reports indicating that concurrent injections of organic gold compounds and antigen resulted in immuno-enhancement that could be measured by direct and indirect plaque-forming cells and rosette-forming cells (Scheiffarth et al 1971;Measel 1975). Indomethacin in the doses used, fully effective in other experimental inflammatory reactions has been unable to modify the cell immigration at the site of challenge.…”
Absfract:The effects of different antirheumatic drugs administered according to various dosing regimes on tuberculin hypersensitivity in rats have been assessed quantitating the changes of exudate volume and mononuclear cells immigration at the site of challenge. Dosing at the time of sensitization with aurothiomalate and D-penicillamine enhanced the cell immigration which was decreased by similar treatment with levamisole. Cyclophosphamide increased the exudate formation. Indomethacin had no effect. Dosing at the time of challenge caused a marked reduction of both the parameters by aurothiomalate and cyclophosphamide and enhancement by levamisole. D-penicillamine increased only the cellular immigration and indomethacin the exudate formation. Long treatment with aurothiomalate and cyclophosphamide suppressed the responses. Similar treatment with D-penicillamine and levamisole produced a significant enhancement. Indomethacin had no effect. The relevance of these findings to the testing and mode of action of antirheumatic drugs is discussed.
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