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Coxsackievirus B4-Induced Cytokine Production in Pancreatic Cells Is Mediated through Toll-Like Receptor 4

机译:柯萨奇病毒B4诱导胰腺细胞中细胞因子的产生通过Toll样受体4介导。

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摘要

Coxsackievirus B4 (CBV4), a member of the Picornavirus genus, has long been implicated in the development of insulin-dependent diabetes mellitus (IDDM) caused by virus-induced pancreatic cell damage. The progressive destruction of pancreatic β cells is responsible for the development of IDDM. It has recently been suggested that CBV4 infection can induce the production of proinflammatory cytokines, and these cytokines seem to be involved in the damage to the insulin-producing cells. In this study we investigated whether toll-like receptors (TLRs) are responsible for triggering the proinflammatory cytokine production in human pancreatic cells in response to CBV4. Here we demonstrate that CBV4 triggers cytokine production through a TLR4-dependent pathway. This interaction seems to be independent of virus attachment and cell entry.
机译:柯萨奇病毒B4(CBV4)是小核糖核酸病毒属的成员,长期以来一直与由病毒引起的胰腺细胞损伤引起的胰岛素依赖型糖尿病(IDDM)的发展有关。胰腺β细胞的逐步破坏是IDDM发展的原因。最近已经提出,CBV4感染可以诱导促炎细胞因子的产生,并且这些细胞因子似乎与胰岛素产生细胞的损伤有关。在这项研究中,我们调查了Toll样受体(TLR)是否负责触发人胰腺细胞响应CBV4促炎性细胞因子的产生。在这里,我们证明CBV4通过TLR4依赖性途径触发细胞因子的产生。这种相互作用似乎与病毒附着和细胞进入无关。

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