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脱氧精胍菌素对小鼠微小膜壳绦虫感染期间效应/记忆T细胞生成的抑制作用。

Inhibitory action of deoxyspergualin on effector/memory T cell generation during Hymenolepis nana infection in mice.

作者信息

Asano K, Muramatsu K, Ikeda K, Okamoto K

机构信息

Department of Medical Biology, School of Medicine, Showa University, Tokyo, Japan.

出版信息

Immunol Lett. 1996 Oct;53(1):51-7. doi: 10.1016/0165-2478(96)02615-6.

DOI:10.1016/0165-2478(96)02615-6
PMID:8946218
Abstract

The effects of deoxyspergualin (DSG), a newly developed immunosuppressive agent, on protective immunity to Hymenolepis nana reinfection were examined in BALB/c mice. Administration of DSG at daily doses of 10.0 mg/kg to 30.0 mg/kg (but not 5.0 mg/kg) caused suppression of protective immunity when the agent was injected intraperitoneally during the induction phase of the immunity. In contrast, daily administration of 30.0 mg/kg DSG, during effector phase, could not suppress protective immunity. DSG inhibited endogenous interferon-gamma production in mesenteric lymph nodes induced by H. nana challenge infection, when the agent was injected intraperitoneally at a daily dose of 10.0 mg/kg during the induction phase of immunity. Delayed type hypersensitivity (DTH) local transfer analysis revealed that administration of DSG at 10.0 mg/kg/day into donor mice during induction phase of immunity inhibited generation of effector/memory cells that mediate DTH to H. nana egg antigen. However, DSG could not inhibit DTH effector cell activation when cells prepared from H. nana-infected, saline-injected mice were transferred into recipient treated with 10.0 mg/kg DSG. Administration of DSG at a dose of 10.0 mg/kg daily for 5 days produced large DNA fragments in mesenteric lymph node (MLN) cells. These results strongly suggest that DSG suppresses generation of effector/memory cells by apoptotic cell death but cannot suppress lymphocyte activation in vivo.

摘要

在BALB/c小鼠中研究了新开发的免疫抑制剂脱氧精胍菌素(DSG)对微小膜壳绦虫再感染的保护性免疫的影响。在免疫诱导期腹腔注射DSG,每日剂量为10.0mg/kg至30.0mg/kg(但不是5.0mg/kg)会导致保护性免疫受到抑制。相比之下,在效应期每日给予30.0mg/kg DSG则不能抑制保护性免疫。当在免疫诱导期腹腔注射每日剂量为10.0mg/kg的DSG时,DSG抑制了由微小膜壳绦虫激发感染诱导的肠系膜淋巴结中内源性γ干扰素的产生。迟发型超敏反应(DTH)局部转移分析显示,在免疫诱导期向供体小鼠每日注射10.0mg/kg DSG会抑制介导对微小膜壳绦虫虫卵抗原的DTH的效应/记忆细胞的产生。然而,当将来自感染微小膜壳绦虫、注射生理盐水的小鼠制备的细胞转移到用10.0mg/kg DSG处理的受体小鼠中时,DSG不能抑制DTH效应细胞的激活。每日以10.0mg/kg的剂量给予DSG,持续5天,会在肠系膜淋巴结(MLN)细胞中产生大片段DNA。这些结果有力地表明,DSG通过凋亡性细胞死亡抑制效应/记忆细胞的产生,但不能在体内抑制淋巴细胞的激活。

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