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正常、免疫接种和传染性腔上囊病病毒(IBDV)感染鸡的腔上囊分泌树突状细胞的糖蛋白产生。

Glycoprotein Production by Bursal Secretory Dendritic Cells in Normal, Vaccinated, and Infectious Bursal Disease Virus (IBDV)-Infected Chickens.

机构信息

Ceva-Phylaxia Ltd., 1107 Budapest, Hungary.

Biovo Animal Health Ltd., 7700 Mohács, Hungary.

出版信息

Viruses. 2022 Jul 30;14(8):1689. doi: 10.3390/v14081689.

Abstract

The aim of this study is to follow the gp production in IBDV-vaccinated and challenged birds. The progress of IBDV infection was monitored using anti-VP2 immunocytochemistry, light and transmission electron microscopy. In the medulla of the bursal follicle, the Movat pentachrome staining discovered an extracellular glycoprotein (gp) produced by bursal secretory dendritic cells (BSDCs). The secretory granules of BSDCs either discharge resulting in extracellular gp or fuse together forming intracellular corpuscles. The double fate of granules suggests a dual function of BSDCs: (a.) For the discharged granules, gp contributes to the medullary microenvironment (ME). (b.) The intracellular corpuscles may be the sign of BSDC transformation to a macrophage-like cell (Mal). Infectious bursal disease virus (IBDV) infection accelerates the BSDC transformation to Mal. The decreased number of BSDCs is feedback for the precursor cells of BSDCs lodging in the cortico-medullary epithelial arches (CMEA), where they proliferate. Opening the CMEA, the precursor cells enter the medulla, and differentiate to immature BSDCs. The virus uptake in the corpuscles prevents the granular discharge resulting in the absence of gp and alteration in ME. In vaccine-take birds, the mitotic rate of BSDC precursor cells cannot restore the precursor pool; therefore, in the case of IBDV challenge, the number of newly formed BSDCs is too low for outbreak of clinical disease. The BSDCs, as a primary target of IBDV, may contribute to the long-lasting immunosuppressive status of IBDV-infected chickens.

摘要

本研究旨在观察 IBDV 疫苗接种和攻毒鸡体内法氏囊生发中心(GC)的生成。采用抗 VP2 免疫细胞化学、光镜和透射电镜观察 IBDV 感染进程。在法氏囊滤泡髓质中,Movat 五重染色发现了由法氏囊分泌性树突状细胞(BSDC)产生的细胞外糖蛋白(gp)。BSDC 的分泌颗粒要么排出导致细胞外 gp,要么融合形成细胞内小体。颗粒的双重命运表明了 BSDC 的双重功能:(a)对于排出的颗粒,gp 有助于髓质微环境(ME)。(b)细胞内小体可能是 BSDC 向巨噬样细胞(Mal)转化的标志。传染性法氏囊病病毒(IBDV)感染加速了 BSDC 向 Mal 的转化。BSDC 数量减少反馈给停泊在皮质-髓质上皮弓(CMEA)中的 BSDC 前体细胞,使其增殖。CMEA 开放,前体细胞进入髓质,分化为未成熟的 BSDC。小体中的病毒摄取阻止了颗粒的排出,导致 gp 缺失和 ME 改变。在疫苗接种鸡中,BSDC 前体细胞的有丝分裂率不能恢复前体细胞池;因此,在 IBDV 攻毒的情况下,新形成的 BSDC 数量太少,不足以引发临床疾病。BSDC 作为 IBDV 的主要靶细胞,可能导致 IBDV 感染鸡的长期免疫抑制状态。

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