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出血性肠炎病毒引起的火鸡淋巴细胞亚群变化及实验性免疫缺陷对病毒发病机制的影响。

Hemorrhagic enteritis virus induced changes in the lymphocyte subpopulations in turkeys and the effect of experimental immunodeficiency on viral pathogenesis.

作者信息

Suresh M, Sharma J M

机构信息

Dept. of Veterinary PathoBiology, College of Veterinary Medicine, University of Minnesota, St. Paul 55108, USA.

出版信息

Vet Immunol Immunopathol. 1995 Mar;45(1-2):139-50. doi: 10.1016/0165-2427(94)05323-k.

Abstract

We examined the changes in the lymphocyte subpopulations in the spleen and peripheral blood of turkeys and the effects of experimental immunodeficiency in the B and T cell compartments on the pathogenesis of hemorrhagic enteritis (HE) in turkeys. Inoculation of turkeys with hemorrhagic enteritis virus (HEV) induced a drop in the relative proportions of IgM bearing cells on Day 2, 3, and 9 post-infection and an elevation in the relative proportions of CD4+ cells on Day 4 and 6 post-infection. Elevated levels of CD8+ cells were observed in the infected turkeys only on Day 16 after infection. Marked depletion of IgM+ cells may play a role in immunodepression caused by HEV. Cyclophosphamide (CY) treatment induced B cell deficiency in turkeys severely impaired HEV replication in the spleen suggesting that B lymphocytes are important for viral replication. Cyclosporin A (CsA) selectively impaired T cell mitogenesis and protected the turkeys against HEV-induced intestinal hemorrhages. CsA did not prevent viral replication in the spleen or the associated splenomegaly. This result suggested that T cell immunity may be important for intestinal hemorrhaging induced by HEV.

摘要

我们研究了火鸡脾脏和外周血中淋巴细胞亚群的变化,以及B细胞和T细胞区室的实验性免疫缺陷对火鸡出血性肠炎(HE)发病机制的影响。用出血性肠炎病毒(HEV)接种火鸡后,感染后第2、3和9天,携带IgM的细胞相对比例下降,感染后第4和6天,CD4 +细胞相对比例升高。仅在感染后第16天,在感染的火鸡中观察到CD8 +细胞水平升高。IgM +细胞的显著减少可能在HEV引起的免疫抑制中起作用。环磷酰胺(CY)处理诱导火鸡B细胞缺陷,严重损害了HEV在脾脏中的复制,表明B淋巴细胞对病毒复制很重要。环孢菌素A(CsA)选择性地损害T细胞有丝分裂,并保护火鸡免受HEV诱导的肠道出血。CsA并未阻止病毒在脾脏中的复制或相关的脾肿大。该结果表明,T细胞免疫可能对HEV诱导的肠道出血很重要。

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