柯萨奇病毒B4诱导胰腺细胞产生细胞因子是通过Toll样受体4介导的。
Coxsackievirus B4-induced cytokine production in pancreatic cells is mediated through toll-like receptor 4.
作者信息
Triantafilou Kathy, Triantafilou Martha
机构信息
School of Life Sciences, JMS Building, University of Sussex, Falmer, Brighton BN1 9QG, United Kingdom.
出版信息
J Virol. 2004 Oct;78(20):11313-20. doi: 10.1128/JVI.78.20.11313-11320.2004.
Abstract
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 beta 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.
摘要
柯萨奇病毒B4（CBV4）是微小核糖核酸病毒属的成员，长期以来一直被认为与病毒诱导的胰腺细胞损伤所导致的胰岛素依赖型糖尿病（IDDM）的发生有关。胰腺β细胞的渐进性破坏是IDDM发生的原因。最近有人提出，CBV4感染可诱导促炎细胞因子的产生，而这些细胞因子似乎参与了对胰岛素产生细胞的损伤。在本研究中，我们调查了Toll样受体（TLR）是否负责触发人胰腺细胞中因CBV4而产生的促炎细胞因子。在此我们证明，CBV4通过TLR4依赖途径触发细胞因子的产生。这种相互作用似乎独立于病毒附着和细胞进入。
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