Immune responses to a soluble schistosomal egg antigen preparation during chronic primary infection with Schistosoma mansoni.
Immune responses to a soluble schistosomal egg antigen preparation during chronic primary infection with Schistosoma mansoni.
复制标题
曼氏血吸虫慢性原发感染期间对可溶性血吸虫卵抗原制剂的免疫反应。
DOI：
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发表时间：
1975
影响因子：
4.4
通讯作者：
Daniel G. Colley
中科院分区：
文献类型：
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作者：
Daniel G. Colley
小鼠曼氏血吸虫病的特点是强烈的，主要是细胞介导的，抗卵，肉芽肿反应，以溶酶体卵抗原（SEA）。抗SEA反应包括淋巴细胞胚细胞生成、产生淋巴因子嗜酸性粒细胞刺激启动子（ESP）、血凝抗体、热不稳定和热稳定的72小时被动皮肤过敏反应（PCA）抗体和明显的外周血嗜酸性粒细胞增多。这些反应在慢性（1年）感染过程中进行了跟踪，并分析了具体参考观察到的肉芽肿形成减少，在持续抗原暴露的存在下，发生在感染后10至12周，并持续在长期血吸虫病。从感染第8周至第50周，淋巴细胞母细胞生成和外周血嗜酸性粒细胞增多呈阳性。在感染8周后的几周内，抗组胺因子的产生和循环热不稳定PCA抗体呈阳性。相比之下，血凝抗体和热稳定的，72小时PCA抗体增加，在第10至14周，并保持在整个慢性感染高。这些对SEA的各种免疫反应的发展和消退表明，有几种潜在的机制可以解释导致这种慢性感染中特异性减少病变形成的免疫调节相互作用。
Murine schistosomiasis mansoni is characterized by an intense, predominantly cell-mediated, anti-egg, granulomatous response to schistosomal egg antigens (SEA). Anti-SEA responses include lymphocyte blastogenesis, the production of the lymphokine eosinophil stimulation promoter (ESP), hemagglutinating antibody, heat-labile and heat-stable, 72-hr passive cutaneous anaphylaxis (PCA) antibodies, and pronounced peripheral blood eosinophilia. These responses were followed during the course of chronic (1 year) infection and analyzed with specific reference to the observed diminution of granuloma formation, in the presence of continued antigenic exposure, which occurs by 10 to 12 weeks after infection and persists during long-term schistosomiasis. Lymphocyte blastogenesis and peripheral blood eosinophilia were positive from the 8th week of infection until the 50th. Lymphokine production and circulating heat-labile PCA antibody were only positive for a few weeks after 8 weeks of infection. In contrast, hemagglutinating antibody and heat-stable, 72-hr PCA antibody increased during weeks 10 to 14 and remained high throughout chronic infection. The development and regression of these various immune responses to SEA indicate that there are several potential mechanisms that could explain the immunoregulatory interactions that result in specifically diminished lesion formation in this chronic infection.