Boros D L, Lukacs N W
Department of Immunology/Microbiology, Wayne State University, School of Medicine, Detroit, MI 48201.
Mem Inst Oswaldo Cruz. 1992;87 Suppl 4:75-9. doi: 10.1590/s0074-02761992000800010.
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 fractionated SEA proteins to elicit granulomas and lymphokine production in infected and egg-immunized mice. At the acute stage of infection SEA fractions (< 21, 25-30, 32-38, 60-66, 70-90, 93-125, and > 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 < 21, 32-38, 40-46, 93-125, and > 200 kD fractions. By 16 days, IL-2 production was evoked 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.(ABSTRACT TRUNCATED AT 250 WORDS)
曼氏血吸虫可溶性虫卵抗原(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,而淋巴因子可调节反应的强度。在本研究中,我们检测了经SDS-PAGE分级的SEA蛋白在感染和虫卵免疫小鼠中引发肉芽肿及产生淋巴因子的能力。在感染急性期,能引发肺部肉芽肿的SEA分级组分(<21、25 - 30、32 - 38、60 - 66、70 - 90、93 - 125和>200 kD)也能引发IL-2、IL-4淋巴因子的产生。在慢性期,能引发肉芽肿的组分数量减少(60 - 66、70 - 90、93 - 125和>200 kD),IL-2、IL-4的产生总体减少。在感染的急性期和慢性期,幼虫-虫卵交叉反应性组分和虫卵特异性组分均能引发肉芽肿。对虫卵免疫小鼠淋巴因子产生情况的检测表明,早在第4天,<21、32 - 38、40 - 46、93 - 125和>200 kD组分刺激的脾细胞就能产生IL-2。到第16天,9个组分中有8个能诱发出IL-2。所有组分在第4天诱导产生的IL-4极少,而在第16天,<21、25 - 30、50 - 56、93 - 125和>200 kD组分能诱发出IL-4。本研究揭示了在感染的急性期和慢性期,能引发肉芽肿及IL-2、IL-4产生所需的SEA分级组分范围存在差异。(摘要截短至250词)