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用艾美耳球虫早熟前体抗原(EPF)进行主动免疫可抑制BALB/c小鼠免疫腹水的形成。

Active immunization with EPF suppresses the formation of immune ascites in BALB/c mice.

作者信息

Quinn K A

机构信息

Department of Surgery, University of Queensland, Royal Brisbane Hospital, Australia.

出版信息

Immunol Cell Biol. 1991 Feb;69 ( Pt 1):1-6. doi: 10.1038/icb.1991.1.

Abstract

The production of early pregnancy factor (EPF) is not confined to pregnancy--EPF has been detected as a product of tumour and transformed cells in vivo and in vitro. In this study, EPF (or an EPF-like substance) was detected also in the serum of BALB/c mice, 7 days after intraperitoneal (i.p.) administration of the mineral oil pristane. Furthermore, EPF was present in serum from mineral oil-induced plasmacytoma-susceptible mice throughout the latent period potentially leading to tumour development, peaking around the time neoplastic cells were identified in ascites. Since mineral oil-induced granuloma is essential to development of immune ascites, involvement of EPF in this process was investigated. Active immunization of BALB/c mice with EPF was shown to suppress the production of immune ascites, induced by multiple i.p. injections of antigen in complete Freund's adjuvant. Of the mice immunized with EPF (n = 19), only 47% produced ascites, compared with 94% of mice receiving saline or human chorionic gonadotrophin and 100% of mice receiving keyhole limpet haemocyanin. Further investigations revealed that ascites was only produced in mice that maintained free-circulating EPF. These mice displayed the classic mineral oil-induced granuloma covering the tissues of the peritoneum. In contrast, the serum of mice that did not produce ascites tested negative for EPF and the peritonea of these mice were devoid of the oil granuloma. These studies suggest that EPF is involved in the initiation and maintenance of the inflammatory response of the peritoneum to mineral oil.

摘要

早期妊娠因子(EPF)的产生并不局限于妊娠——在体内和体外,EPF已被检测为肿瘤和转化细胞的产物。在本研究中,腹腔注射角鲨烯后7天,在BALB/c小鼠的血清中也检测到了EPF(或一种EPF样物质)。此外,在矿物油诱导的浆细胞瘤易感小鼠的血清中,在可能导致肿瘤发展的整个潜伏期都存在EPF,在腹水液中发现肿瘤细胞时达到峰值。由于矿物油诱导的肉芽肿对于免疫腹水的发展至关重要,因此研究了EPF在这一过程中的作用。结果表明,用EPF对BALB/c小鼠进行主动免疫可抑制完全弗氏佐剂中多次腹腔注射抗原所诱导的免疫腹水的产生。在用EPF免疫的小鼠(n = 19)中,只有47%产生了腹水,相比之下,接受生理盐水或人绒毛膜促性腺激素的小鼠为94%,接受钥孔戚血蓝蛋白的小鼠为100%。进一步的研究表明,只有在维持游离循环EPF的小鼠中才会产生腹水。这些小鼠表现出覆盖腹膜组织的典型矿物油诱导肉芽肿。相反,未产生腹水的小鼠血清中EPF检测呈阴性,且这些小鼠的腹膜没有油肉芽肿。这些研究表明,EPF参与了腹膜对矿物油炎症反应的启动和维持。

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