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Roles of PAR1 and PAR2 in viral myocarditis

机译:PAR1和PAR2在病毒性心肌炎中的作用

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摘要

Viral myocarditis is estimated to cause ~ 20% of sudden death in people under the age of 40. A variety of viruses have been found to cause myocarditis including coxsackievirus B3 (CVB3). Many studies have been performed with CVB3 because there is a mouse model of CVB3-induced myocarditis. Studies have shown that the TLR3-IFNβ pathway plays a central role in the innate immune response to CVB3 infection. Our laboratory studies the role of protease activated receptors (PAR) in different biological responses including viral infection. We examined the effect of a deficiency in either PAR1 or PAR2 on CVB3-induced myocarditis. Interestingly, we found that PAR1 knockout mice had increased cardiac injury whereas PAR2 knockout mice had decreased cardiac injury. Our studies support the notion that PARs modulate the innate immune response and can have both positive and negative effects on TLR-dependent responses.
机译:在40岁以下的人群中,病毒性心肌炎估计会导致约20%的猝死。已发现多种病毒可引起心肌炎,包括柯萨奇病毒B3(CVB3)。由于存在CVB3诱发的心肌炎的小鼠模型,因此对CVB3进行了许多研究。研究表明,TLR3-IFNβ途径在对CVB3感染的天然免疫应答中起着核心作用。我们的实验室研究了蛋白酶激活受体(PAR)在包括病毒感染在内的不同生物学反应中的作用。我们检查了PAR1或PAR2缺乏对CVB3引起的心肌炎的影响。有趣的是,我们发现PAR1基因敲除小鼠心脏损伤增加,而PAR2基因敲除小鼠心脏损伤减少。我们的研究支持以下观点:PAR调节先天性免疫应答,并且对TLR依赖性应答具有正反作用。

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