Coxsackievirus infection of the pancreas: Evaluation of receptor expression, pathogenesis, and immunopathology
Coxsackievirus infection of the pancreas: Evaluation of receptor expression, pathogenesis, and immunopathology
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DOI：
10.1006/viro.2000.0332
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发表时间：
2000-06-05
期刊：
影响因子：
3.7
通讯作者：
Whitton, JL
中科院分区：
文献类型：
--
作者：
Mena, I;Fischer, C;Whitton, JL
柯萨奇病毒B型（CVB）感染胰腺诱导由自然杀伤细胞、T细胞和巨噬细胞组成的大量细胞浸润，并导致外分泌组织的破坏。胰腺CVB感染的生理表现与病毒嗜性相关;病毒感染腺泡细胞，但不感染胰岛。在这里，我们评估胰腺炎症和破坏的机制，并确定病毒嗜性的决定因素。T细胞介导的免疫病理学，沿着直接的病毒介导的细胞病变，被用来解释CVB诱导的胰腺疾病的某些方面。然而，我们在这里表明，在胰腺中，炎症和组织破坏的程度似乎没有改变的情况下的溶细胞蛋白穿孔素，这些研究结果排除任何要求穿孔素介导的裂解自然杀伤细胞或细胞毒性T细胞在CVB 3诱导的胰腺损伤。此外，穿孔素介导的细胞毒性T细胞活性并不有助于控制该器官中的CVB感染。此外，我们证明，最近确定的柯萨奇-腺病毒受体在腺泡细胞中表达水平很高，但在胰岛中几乎检测不到，这与其作为病毒嗜性的主要决定因素是一致的，因此，疾病。然而，使用胰腺来源的各种细胞系的进一步研究揭示了病毒嗜性的次要决定因素。(C)北京大学出版社.
Coxsackievirus type B (CVB) infection of the pancreas induces a massive cellular infiltrate composed of natural killer cells, T cells, and macrophages and leads to the destruction of exocrine tissue. The physiological manifestations of pancreatic CVB infection are correlated with viral tropism; the virus infects acinar cells but spares the islets of Langerhans. Here we evaluate the mechanisms underlying pancreatic inflammation and destruction and identify the determinants of viral tropism. T-cell-mediated immunopathology has been invoked, along with direct virus-mediated cytopathicity, to explain certain aspects of CVB-induced pancreatic disease. However, we show here that in the pancreas, the extent of inflammation and tissue destruction appears unaltered in the absence of the cytolytic protein perforin; these findings exclude any requirement for perforin-mediated lysis by natural killer cells or cytotoxic T cells in CVB3-induced pancreatic damage. Furthermore, perforin-mediated cytotoxic T-cell activity does not contribute to the control of CVB infection in this organ. In addition, we demonstrate that the recently identified coxsackie-adenovirus receptor is expressed at high levels in acinar cells but is barely detectable in islets, which is consistent with its being a major determinant of virus tropism and, therefore, of disease. However, further studies using various cell lines of pancreatic origin reveal secondary determinants of virus tropism. (C) 2000 Academic Press.