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巨噬细胞在农药暴露和原生动物感染小鼠中诱导T抑制细胞。

Macrophage induction of T-suppressor cells in pesticide-exposed and protozoan-infected mice.

作者信息

Loose L D

出版信息

Environ Health Perspect. 1982 Feb;43:89-97. doi: 10.1289/ehp.824389.

Abstract

The use of infectious pathogens has allowed the detection of the development of synergism between pathogens and ubiquitous environmental chemical contaminants. This synergism has been demonstrated to result in a state of immunosuppression which either did not occur in the independent and singular presence of the chemical or pathogen and/or was greater than additive when both were combined. The immunosuppression was distinct with regard to the organochloride used and, therefore, is not a ubiquitous characteristic of all organohalides. The production of a macrophage soluble factor which appeared to induce T-suppressor cells was demonstrated in hepatic Kupffer cells from mice administered 5 ppm of dieldrin for 10 weeks and then infected with Leishmania tropical promastigotes. The factor was not generated in mice administered dieldrin and infected with malaria nor in mice administered only dieldrin nor in mice only infected with Leishmania. Additional studies revealed a profound impairment in macrophage antigen processing with macrophages obtained from mice administered dieldrin. The use of pathogen models may allow the immunosuppressive potential of environmental chemical contaminants to be expressed in a more sensitive manner.

摘要

使用传染性病原体已能够检测病原体与普遍存在的环境化学污染物之间协同作用的发展情况。这种协同作用已被证明会导致免疫抑制状态,这种状态在化学物质或病原体单独存在时不会出现,和/或在两者结合时大于相加效应。所使用的有机氯导致的免疫抑制是不同的,因此,并非所有有机卤化物都具有普遍特征。在给小鼠施用5 ppm狄氏剂10周后再感染热带利什曼原虫前鞭毛体,从小鼠肝脏库普弗细胞中证实产生了一种似乎能诱导T抑制细胞的巨噬细胞可溶性因子。在施用狄氏剂并感染疟疾的小鼠中、仅施用狄氏剂的小鼠中或仅感染利什曼原虫的小鼠中均未产生该因子。进一步的研究表明,从施用狄氏剂的小鼠获得的巨噬细胞在抗原加工方面存在严重缺陷。使用病原体模型可能会使环境化学污染物的免疫抑制潜力以更敏感的方式表现出来。

相似文献

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Virus-pesticide interactions with murine cellular immunity after sublethal exposure to dieldrin and aminocarb.
J Toxicol Environ Health. 1988;25(1):103-18. doi: 10.1080/15287398809531192.

引用本文的文献

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Immunotoxicology--current concepts.
Surv Immunol Res. 1983;2(3):318-20. doi: 10.1007/BF02918443.
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