Network interactions in Schistosoma japonicum infection. Identification and characterization of a serologically distinct immunoregulatory auto-antiidiotypic antibody population.
Network interactions in Schistosoma japonicum infection. Identification and characterization of a serologically distinct immunoregulatory auto-antiidiotypic antibody population.
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日本血吸虫感染中的网络相互作用。
DOI：
10.1172/jci112245
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Kresina,TF
中科院分区：
文献类型：
--
作者：
Olds,GR;Kresina,TF
本研究探讨了天然存在的抗独特型抗体（抗 id）在日本血吸虫感染期间血清抑制中的作用，该抗体对血吸虫卵抗原（SEA）抗体上的表位具有特异性。在感染 12、16 和 30 周时从感染血清池中获得了三种抗 id 制剂。抗id（12周）结合36%的标记抗SEA抗体，具有5微克/ml的独特型结合能力（IBC），并且不抑制SEA诱导的增殖。抗id（16周）结合了17%的标记抗SEA抗体，具有29微克IBC/ml，并且3H掺入从21.4+/-0.5（10微克/ml正常Ig）减少到9.1+/-1.5 X 10(4)cpm（P小于0.01）。抗id（30周）结合66%的标记抗SEA抗体，具有84微克IBC/ml，并抑制3H掺入88%（4.8+/-0.3 X 10(4)cpm，P小于0.001）。对这三个抗独特型抗体群的血清学反应性分析表明，抗-id（12周）描述了含有次要交叉反应独特型（SJ-CRIm）的抗SEA分子独特型群。相比之下，抗-id（30周）描述了一个血清学上不同的独特型群体，其中含有主要的交叉反应独特型抗-SEA分子（SJ-CRIM）。一种单克隆抗 id 与超过 50% 的描述 SJ-CRIM 的抗 SEA 分子发生反应，在体外具有显着的抑制作用，并将体内寄生虫卵周围的肉芽肿炎症从 113 X 10(3) micron2 减少到 23 X 10(3) micron2（80% 抑制，P 小于 0.001）。这些观察结果表明，免疫网络相互作用调节慢性鼠日本血吸虫感染的炎症。
This study examined the role of naturally occurring anti-idiotypic antibody (anti-id), specific for epitopes on antibodies to schistosome egg antigens (SEA), in serosuppression during Schistosoma japonicum infection. Three anti-id preparations were obtained from pools of infected serum at 12, 16, and 30 wk of infection. Anti-id (12 wk) bound 36% of labeled anti-SEA antibodies, had an idiotype binding capacity (IBC) of 5 micrograms/ml, and did not suppress SEA-induced proliferation. Anti-id (16 wk) bound 17% of labeled anti-SEA antibodies, had 29 micrograms IBC/ml, and reduced 3H incorporation from 21.4 +/- 0.5 (10 micrograms/ml normal Ig) to 9.1 +/- 1.5 X 10(4) cpm (P less than 0.01). Anti-id (30 wk) bound 66% of labeled anti-SEA antibody, had 84 micrograms IBC/ml, and suppressed 3H incorporation by 88% (4.8 +/- 0.3 X 10(4) cpm, P less than 0.001). Analysis of the serologic reactivity of these three populations of anti-idiotypic antibodies revealed that anti-id (12 wk) described an idiotypic population of anti-SEA molecules containing a minor cross-reactive idiotype (SJ-CRIm). In contrast, anti-id (30 wk) described a serologically distinct, idiotypic population containing a major cross-reactive idiotype of anti-SEA molecules (SJ-CRIM). A monoclonal anti-id, which reacted with greater than 50% of the anti-SEA molecules describing SJ-CRIM, was profoundly suppressive in vitro and reduced granulomatous inflammation around parasite eggs in vivo from 113 X 10(3) micron2 to 23 X 10(3) micron2 (80% suppression, P less than 0.001). These observations suggest that immune network interactions modulate inflammation in chronic murine S. japonicum infection.
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