Montesano M A, Freeman G L, Gazzinelli G, Colley D G
Universidade Federal de Juiz de Fora, Juiz de Fora MG, Brazil.
J Immunol. 1990 Aug 1;145(3):1002-8.
Immunoaffinity-purified antibodies against Schistosoma mansoni soluble egg Ag (SEA) from infected patients' sera differ idiotypically according to the donor's clinical form of the disease. The Id differ both by their ability to stimulate proliferation of anti-Id T cells and their recognition by anti-Id-specific sera. Also, mice infected with S. mansoni develop anti-Id T and B cell responses against mouse anti-SEA antibodies. We now show that anti-SEA antibodies from serum pools of chronic, but asymptomatic patients (AM1 and AM5) stimulate proliferation of spleen cells from mice infected with S. mansoni. However, AM8, anti-SEA antibodies from hepatosplenic patients, did not stimulate these spleen cells. The murine responses directly parallel patient studies where AM1 and AM5 Id-stimulated human PBMC, but AM8 Id did not. In competitive ELISA, using AM1 or AM-5-specific rabbit antisera or human anti-SEA mAb E5-specific rabbit antiserum, sera from mice infected for 8 and 16 wk (but not from uninfected mice) compete with AM1, AM5, or E5. These sera do not compete in the AM8/anti-AM8 competitive ELISA. Sera from 8-wk-infected mice inhibit more against AM1, AM5, and E5 than do sera from later infections, and anti-SEA immunoaffinity-purified antibodies from 8-wk-infected mice stimulate spleen cells from infected mice more than anti-SEA antibodies from sera of mice late in infection. However, spleen cells from more chronically infected mice are more responsive to either the murine or human anti-SEA antibody preparations than cells from mice with earlier infections. Both the ELISA data and lymphocyte responses indicate that anti-SEA antibodies from mice infected with S. mansoni for 8 wk bear Id cross-reactive with those expressed on anti-SEA antibodies from humans with chronic, asymptomatic schistosomiasis, but not those from hepatosplenic patients.
从感染患者血清中通过免疫亲和纯化获得的抗曼氏血吸虫可溶性虫卵抗原（SEA）抗体，其独特型会因疾病的临床类型不同而有所差异。这些独特型在刺激抗独特型T细胞增殖的能力以及被抗独特型特异性血清识别方面均存在差异。此外，感染曼氏血吸虫的小鼠会针对小鼠抗SEA抗体产生抗独特型T细胞和B细胞反应。我们现在发现，来自慢性但无症状患者（AM1和AM5）血清池的抗SEA抗体可刺激感染曼氏血吸虫小鼠的脾细胞增殖。然而，来自肝脾型患者的AM8抗SEA抗体却不能刺激这些脾细胞。小鼠的反应与患者研究直接平行，在患者研究中，AM1和AM5独特型可刺激人外周血单个核细胞（PBMC），但AM8独特型却不能。在竞争性ELISA中，使用AM1或AM - 5特异性兔抗血清或人抗SEA单克隆抗体E5特异性兔抗血清时，感染8周和16周的小鼠血清（但未感染小鼠的血清不会）可与AM1、AM5或E5发生竞争。这些血清在AM8/抗AM8竞争性ELISA中不发生竞争。感染8周小鼠的血清对AM1、AM5和E5的抑制作用比后期感染小鼠的血清更强，并且来自感染8周小鼠血清的抗SEA免疫亲和纯化抗体比感染后期小鼠血清中的抗SEA抗体更能刺激感染小鼠的脾细胞。然而，慢性感染时间更长的小鼠的脾细胞比早期感染小鼠的细胞对鼠源或人源抗SEA抗体制剂的反应更强。ELISA数据和淋巴细胞反应均表明，感染曼氏血吸虫8周的小鼠的抗SEA抗体所携带的独特型与慢性无症状血吸虫病患者的抗SEA抗体上表达的独特型具有交叉反应性，但与肝脾型患者的抗SEA抗体的独特型无交叉反应。
