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Rheumatoid factor activity in four patients was not inhibited by infusions of large volumes of plasma and gamma globulin as measured by the Hyland latex, SHC, and SSC tests. There were also no demonstrable changes in the erythrocyte sedimentation rates, total serum proteins, electrophoretic patterns, and ultracentrifuge patterns. In vitro estimations showed that very large amounts of gamma globulin would be needed to achieve in vivo inhibition of rheumatoid factor activity.In quatro subjectos le activitate de factor rheumatoide non esseva inhibite per infusiones de grande quantitates de plasma e de globulina gamma, a judicar per le resultatos de tests a latex de Hyland, de sensibilisate cellulas human, e de sensibilisate cellulas ovin. In plus, nulle demonstrabile alterationes esseva trovate in le velocitate del sedimentation de erythrocytos, le totales de proteina seral, le configuration electrophoretic, e le configuration de ultracentrifugage.Estimationes in vitro monstrava que grandissime quantitates de globulina gamma esserea requirite pro effectuar un inhibition in vivo del activitate de factor rheumatoide. HE DEMONSTRATION that rheumatoid factors react with gammaT globulin and the finding that gamma globulin fractions of normal sera inhibit rheumatoid factor activity have given rise to the concept that rheumatoid factors are anti-gamma globulin antibodies.In 1954 Heller et a1.l found that Cohn fraction I1 (gamma globulin) from human sera inhibited the agglutination reactions of rheumatoid sera. He then developed the F I1 test based on the premise that human gamma globulin had affinity for rheumatoid factor. Further, Epstein et aL2 emphasized the correlation between the amount of rheumatoid factor as measured by the formation of precipitates on addition of fraction I1 and F I1 (tanned cell) agglutination titer. Grubb3p4 showed that certain normal sera inbibit the reaction between agglutinating factors in rheumatoid sera and sensitized Rh positive cells.The possibility that altered gamma globulins are the antigens which stimulate formation of rheumatoid factors is suggested by certain findings. Christian et aL5 found that aggregated gamma globulin readily precipitated with most rheumatoid sera, and in' low concentrations inhibited the F I1 tanned sheep cell agglutination test. Milgrom et a1.6 demonstrated in certain normal sera what he considered to be antibodies to "immune" globulin. These antibodies were neutralized by anti-Rh antibodies eluted from red cells, but not by
Rheumatoid factor activity in four patients was not inhibited by infusions of large volumes of plasma and gamma globulin as measured by the Hyland latex, SHC, and SSC tests. There were also no demonstrable changes in the erythrocyte sedimentation rates, total serum proteins, electrophoretic patterns, and ultracentrifuge patterns. In vitro estimations showed that very large amounts of gamma globulin would be needed to achieve in vivo inhibition of rheumatoid factor activity.In quatro subjectos le activitate de factor rheumatoide non esseva inhibite per infusiones de grande quantitates de plasma e de globulina gamma, a judicar per le resultatos de tests a latex de Hyland, de sensibilisate cellulas human, e de sensibilisate cellulas ovin. In plus, nulle demonstrabile alterationes esseva trovate in le velocitate del sedimentation de erythrocytos, le totales de proteina seral, le configuration electrophoretic, e le configuration de ultracentrifugage.Estimationes in vitro monstrava que grandissime quantitates de globulina gamma esserea requirite pro effectuar un inhibition in vivo del activitate de factor rheumatoide. HE DEMONSTRATION that rheumatoid factors react with gammaT globulin and the finding that gamma globulin fractions of normal sera inhibit rheumatoid factor activity have given rise to the concept that rheumatoid factors are anti-gamma globulin antibodies.In 1954 Heller et a1.l found that Cohn fraction I1 (gamma globulin) from human sera inhibited the agglutination reactions of rheumatoid sera. He then developed the F I1 test based on the premise that human gamma globulin had affinity for rheumatoid factor. Further, Epstein et aL2 emphasized the correlation between the amount of rheumatoid factor as measured by the formation of precipitates on addition of fraction I1 and F I1 (tanned cell) agglutination titer. Grubb3p4 showed that certain normal sera inbibit the reaction between agglutinating factors in rheumatoid sera and sensitized Rh positive cells.The possibility that altered gamma globulins are the antigens which stimulate formation of rheumatoid factors is suggested by certain findings. Christian et aL5 found that aggregated gamma globulin readily precipitated with most rheumatoid sera, and in' low concentrations inhibited the F I1 tanned sheep cell agglutination test. Milgrom et a1.6 demonstrated in certain normal sera what he considered to be antibodies to "immune" globulin. These antibodies were neutralized by anti-Rh antibodies eluted from red cells, but not by
Because agammaglobulinemic patients show a markedly increased incidence of a rheumatoid‐like arthritis, which improves after γ globulin treatment, the clinical and serological changes resulting from repeated injections of pooled human γ globulin given to adult patients with rheumatoid arthritis have been evaluated in a controlled, double‐blind study. No significant beneficial effects on laboratory or clinical parameters were observed. However, 2 of the 10 patients treated developed precipitating antibody to a β globulin component of the γ globulin preparation given.
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