Parra J C, Gazzinelli G, Goes A M, Moyes R B, Rocha R, Colley D G, Doughty B L
Centro de Pesquisas Rene Rachou, FIOCRUZ, Belo Horizonte, Brazil.
J Immunol. 1991 Dec 1;147(11):3949-54.
We have previously reported on Id/anti-Id-receptor interactions in clinical human schistosomiasis. These findings support a hypothesis that anti-SEA cross-reactive Id develop in some patients during the course of a chronic infection and participate in regulation of anti-SEA cellular immune responses. We report here on experiments that extend those observations to the regulation of granulomatous hypersensitivity measured by an in vitro granuloma model. T cells from chronic intestinal schistosomiasis patients were stimulated in vitro with anti-SEA Id and assayed in an autologous in vitro granuloma assay for modulation of granuloma formation. These anti-SEA Id-reactive T cells were capable of regulating autologous in vitro granuloma formation. Both CD4 and CD8 T cells could be activated to regulate granuloma formation. This regulatory activity, initiated with stimulatory anti-SEA idiotypic antibodies, was antigenically specific and was dependent on the presence of intact F(ab')2 Ig molecules. The ability to elicit this regulatory activity appears to be dose dependent and is more easily demonstrated in chronically infected intestinal patients or SEA-sensitized individuals. These data support the hypothesis that anti-SEA cross-reactive Id are important in regulating granulomatous hypersensitivity in chronic intestinal schistosomiasis patients and these cross-reactive Id appear to play a major role in cell-cell interactions that result in the regulation of anti-SEA cellular immune responses.
我们之前曾报道过临床人类血吸虫病中Id/抗Id受体的相互作用。这些发现支持了一种假说，即在慢性感染过程中，一些患者会产生抗SEA交叉反应性Id，并参与抗SEA细胞免疫反应的调节。我们在此报告了一些实验，这些实验将这些观察结果扩展到通过体外肉芽肿模型测量的肉芽肿性超敏反应的调节。来自慢性肠道血吸虫病患者的T细胞在体外用抗SEA Id刺激，并在自体体外肉芽肿试验中检测对肉芽肿形成的调节作用。这些抗SEA Id反应性T细胞能够调节自体体外肉芽肿的形成。CD4和CD8 T细胞均可被激活以调节肉芽肿的形成。这种由刺激性抗SEA独特型抗体引发的调节活性具有抗原特异性，并且依赖于完整的F(ab')2 Ig分子的存在。引发这种调节活性的能力似乎具有剂量依赖性，并且在慢性感染的肠道患者或SEA致敏个体中更容易得到证实。这些数据支持了这样一种假说，即抗SEA交叉反应性Id在调节慢性肠道血吸虫病患者的肉芽肿性超敏反应中很重要，并且这些交叉反应性Id似乎在导致抗SEA细胞免疫反应调节的细胞间相互作用中起主要作用。
