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首页> 外文期刊>Memórias do Instituto Oswaldo Cruz >The role of egg antigens, cytokines in granuloma formation in murine schistosomiasis mansoni
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The role of egg antigens, cytokines in granuloma formation in murine schistosomiasis mansoni

机译:鸡蛋抗原,细胞因子在曼氏血吸虫病肉芽肿形成中的作用

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摘要

The induction of granuloma formation by soluble egg antigens (SEA) of Schistosoma mansoni is accompanied by T cell-mediated lymphokine production that regulates the intensity of the response. In the present study we have examined the ability of SDS-PAGE fractioned SEA proteins to elicit granulomas and lymphokine production in infected and egg-immunized mice. At the acute stage of infection SEA fractions ( 200 kD) that elicited pulmonary granulomas also elicited IL-2, IL-4 lymphokine production. At the chronic stage a diminished number of fractions (60-66, 70-90, 93-125, and > 200 kD) were able to elicit granulomas with an overall decrease in IL-2, IL-4 production. Granulomas were elicited by larval-egg crossreactive and egg-specific fractions at both the acute and chronic stage of the infection. Examination of lymphokine production from egg-immunized mice demonstrated that as early as 4 days IL-2 was produced by spleen cells stimulated with 200 kD fractions. By 16 days, IL-2production was envoked by 8 of 9 fractions. IL-4 production at 4 days in response to all fractions was minimal while at 16 days IL-4 was elicited with the < 21, 25-30, 50-56, 93-125, and > 200 kD fractions. The present study reveals differences in the range of SEA fractions able to elicit granulomas and IL-2, IL-4 production between acute and chronic stages of infection. Additionally, this study demonstrates sequential (IL-2 followed by IL-4) lymphokine production during the primary egg antigen response.
机译:曼氏血吸虫的可溶性卵抗原(SEA)诱导肉芽肿形成的过程伴随着T细胞介导的淋巴因子产生,从而调节反应强度。在本研究中,我们已经检查了SDS-PAGE分离SEA蛋白在感染和卵免疫小鼠中引起肉芽肿和淋巴因子产生的能力。在感染的急性期,引发肺肉芽肿的SEA分数(200 kD)也引起IL-2,IL-4淋巴因子的产生。在慢性阶段,级分数量减少(60-66、70-90、93-125和> 200 kD)能够引发肉芽肿,而IL-2,IL-4产生量总体下降。在感染的急性和慢性阶段,幼虫-卵的交叉反应性和卵特异性级分均引起肉芽肿。对卵免疫小鼠的淋巴因子产生的检查表明,早在4天时,用200 kD组分刺激的脾细胞就产生了IL-2。到16天时,9个馏分中的8个引起了IL-2的产生。响应所有馏分的第4天的IL-4产生极少,而第16天时,<21、25-30、50-56、93-125和> 200 kD馏分引发IL-4。本研究揭示了在急性和慢性感染阶段之间能够引发肉芽肿和SE-2,IL-4产生的SEA分数范围的差异。此外,这项研究表明在原代卵抗原反应过程中顺序产生(IL-2,然后是IL-4)淋巴因子。

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