Cox H W, Hayes M M, Saleh S M
J Parasitol. 1984 Feb;70(1):57-62.
Fresh plasma from rats infected with Trypanosoma brucei rhodesiense, incubated with splenic lymphocytes from rats previously immunized with sheep blood cells, suppressed the capacity of the splenic lymphocytes to produce antibody as was indicated by reductions in the numbers of hemolytic Jerne plaques produced by the treated cells. The effect was maximal in plasma samples drawn on the sixth to eighth day of infection when they contained elevated amounts of soluble immune complex, high titers of immunoconglutinin (IK), and reduced titers of lytic complement. We suggest that the active plasma may have affected the antibody-producing cells by one or both of two mechanisms. Soluble antigen-antibody complexes may have interacted with Fc receptors of activated lymphocytes to suppress antibody production. Alternatively, complement-fixing soluble immune complexes may have reacted with C3b receptors of the lymphocytes. These lymphocytes coated with the antigen for IK could then be injured by immunoconglutination.
用罗得西亚布氏锥虫感染的大鼠的新鲜血浆,与先前用绵羊血细胞免疫的大鼠的脾淋巴细胞一起孵育,结果表明处理后的细胞产生的溶血耶尔恩斑数量减少,从而抑制了脾淋巴细胞产生抗体的能力。在感染的第六至第八天采集的血浆样本中,这种效应最为明显,此时血浆中含有升高的可溶性免疫复合物、高滴度的免疫粘连素(IK)和降低的溶细胞补体滴度。我们认为,活性血浆可能通过两种机制中的一种或两种来影响抗体产生细胞。可溶性抗原 - 抗体复合物可能与活化淋巴细胞的Fc受体相互作用以抑制抗体产生。或者,补体结合性可溶性免疫复合物可能与淋巴细胞的C3b受体发生反应。这些被IK抗原包被的淋巴细胞随后可能因免疫粘连而受损。