PRODUCTION OF INTERLEUKIN-1 (IL-1) AND IL-1 INHIBITOR BY HUMAN MONOCYTES EXPOSED TO DENGUE VIRUS
PRODUCTION OF INTERLEUKIN-1 (IL-1) AND IL-1 INHIBITOR BY HUMAN MONOCYTES EXPOSED TO DENGUE VIRUS
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DOI：
10.1093/infdis/170.4.811
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发表时间：
1994-10-01
影响因子：
6.4
通讯作者：
SHAIO, MF
中科院分区：
文献类型：
--
作者：
CHANG, DM;SHAIO, MF
登革出血热-登革休克综合征是急性登革病毒（DV）感染的最严重表现，在东南亚流行。单核吞噬细胞中DV生长的抗体依赖性增强被认为是先前存在的登革热抗体赋予这种结果过度风险的机制。白细胞介素-1 （IL-1）可能在引起登革热和休克的发病机制中起重要作用。结果表明，在DV感染后的4小时内，白细胞介素-1和肿瘤坏死因子- α均由单核细胞分泌。然而，与健康对照相比，登革热患者受病毒刺激的单核细胞分泌IL-1没有增加。在聚集的免疫球蛋白或免疫复合物存在的情况下，dv感染的单核细胞分泌大量的IL-1。此外，从感染dv的单核细胞的上清液中鉴定出一种新的600 kda的IL-1抑制剂。该抑制剂可引起免疫抑制，影响DV感染过程。
Dengue hemorrhagic fever-dengue shock syndrome, the most severe manifestation of an acute dengue virus (DV) infection, is endemic in Southeast Asia. Antibody-dependent enhancement of DV growth in mononuclear phagocytes is thought to be the mechanism whereby preexisting dengue antibodies confer excess risk for this outcome. Interleukin-1 (IL-1) may play an important role in the pathogenetic mechanisms that cause dengue fever and shock. It was shown that both IL-1 and tumor necrosis factor-alpha are secreted from monocytes within 4 h after DV infection. However, there was no increase in IL-1 secretion by virus-stimulated monocytes from dengue fever patients compared with healthy controls. Significant amounts of IL-1 were secreted by DV-infected monocytes in the presence of aggregated immunoglobulin or immune complexes, In addition, a new 600-kDa IL-1 inhibitor from the supernatants of DV-infected monocytes was identified. This inhibitor may cause immunosuppression and influence the process of DV infection.