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首页> 外文期刊>Nature immunology >CD8(+) T cells induce cachexia during chronic viral infection
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CD8(+) T cells induce cachexia during chronic viral infection

机译:CD8(+)T细胞在慢性病毒感染期间诱发恶病症

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摘要

Cachexia represents a leading cause of morbidity and mortality in various cancers, chronic inflammation and infections. Understanding of the mechanisms that drive cachexia has remained limited, especially for infection-associated cachexia (IAC). In the present paper we describe a model of reversible cachexia in mice with chronic viral infection and identify an essential role for CD8(+) T cells in IAC. Cytokines linked to cancer-associated cachexia did not contribute to IAC. Instead, virus-specific CD8(+) T cells caused morphologic and molecular changes in the adipose tissue, which led to depletion of lipid stores. These changes occurred at a time point that preceded the peak of the CD8(+) T cell response and required Tcell-intrinsic type I interferon signaling and antigen-specific priming. Our results link systemic antiviral immune responses to adipose-tissue remodeling and reveal an underappreciated role of CD8(+) T cells in IAC.
机译:辣味群岛代表了各种癌症,慢性炎症和感染中发病率和死亡率的主要原因。 了解驱动恶病症的机制仍然有限,特别是对于感染相关的恶病症(IAC)。 在本文中,我们描述了具有慢性病毒感染的小鼠可逆性恶病毒模型,并确定IAC中CD8(+)T细胞的基本作用。 与癌症相关的恶病症相关的细胞因子对IAC没有贡献。 相反,病毒特异性CD8(+)T细胞导致脂肪组织的形态学和分子变化,导致脂质储存的枯竭。 这些变化发生在CD8(+)T细胞响应峰的峰值之前的时间点和所需的TCell内在类型I干扰素信号传导和抗原特异性引发。 我们的结果将全身抗病毒免疫应答链接到脂肪组织重塑,并揭示了IAC中CD8(+)T细胞的低估作用。

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