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实验性传染性法氏囊病中血液学变化、血清及单核细胞抑制与淋巴细胞对植物血凝素刺激早期抑制的相关性

Correlation of hematological changes and serum and monocyte inhibition with the early suppression of phytohemagglutinin stimulation of lymphocytes in experimental infectious bursal disease.

作者信息

Confer A W, MacWilliams P S

出版信息

Can J Comp Med. 1982 Apr;46(2):169-75.

Abstract

Several experiments were conducted to study the mechanism of infectious bursal disease virus induced suppression of phytohemagglutinin stimulation of peripheral blood lymphocytes. Infectious bursal disease virus inoculation of one week old chicks resulted in significant suppression of phytohemagglutinin stimulation during the first three days after inoculation as demonstrated by a whole blood assay. Mild thymic necrosis was seen on day 3. Hematological changes during this time consisted of increased numbers of circulating lymphocytes and monocytes in infected chickens. Absolute monocyte counts remained elevated even after phytohemagglutinin stimulation had returned to normal. Furthermore, even after a 72.3% reduction in the monocyte population in leukocyte preparations, there was still marked viral induced suppression of phytohemagglutinin stimulation. An elevation in the absolute number of circulating large immature lymphocytes correlated with suppression of phytohemagglutinin stimulation. Sera from infected and control chickens depressed phytohemagglutinin stimulation of lymphocytes from control chickens at the 5 and 10% concentration. At the 1% concentration, inhibiton by control sera was considerably less than the inhibition by infected sera. The relationship between these findings and the mechanism of viral induced suppression of T-lymphocyte function is discussed.

摘要

进行了多项实验以研究传染性法氏囊病病毒诱导外周血淋巴细胞对植物血凝素刺激反应受抑制的机制。对1周龄雏鸡接种传染性法氏囊病病毒,通过全血检测发现,接种后的头三天,植物血凝素刺激反应受到显著抑制。在第3天可见轻度胸腺坏死。在此期间,感染鸡的血液学变化包括循环淋巴细胞和单核细胞数量增加。即使植物血凝素刺激反应恢复正常后,绝对单核细胞计数仍保持升高。此外,即使白细胞制剂中的单核细胞数量减少了72.3%,病毒诱导的植物血凝素刺激反应抑制仍很明显。循环中大型未成熟淋巴细胞绝对数量的增加与植物血凝素刺激反应的抑制相关。来自感染鸡和对照鸡的血清在5%和10%浓度时可抑制对照鸡淋巴细胞对植物血凝素的刺激反应。在1%浓度时,对照血清的抑制作用明显小于感染血清。本文讨论了这些发现与病毒诱导T淋巴细胞功能抑制机制之间的关系。

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