组织组织和稳态对癌症炎症细胞骨架信号传导的影响

A. Ahmadi
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引用次数: 0

摘要

组织组织和体内平衡是建立在一系列回路的基础上的,其中包括调节组织环境的炎症信号。这些连接的失衡可能导致炎症性疾病和免疫系统的抑制,如慢性病毒感染和癌症[1]。干扰素I型(IFN-Is)是病毒感染细胞产生的关键刺激物,在邻近细胞中产生固有的细胞抗病毒状态以消除感染。然而,长期IFN-I信号通过诱导损害免疫的抑制剂来促进组织组织和体内平衡,从而导致免疫功能受损[2]。这些连接的不平衡可能导致炎症性疾病和免疫抑制,如慢性病毒感染和癌症,干扰素I型(IFN-Is)是细胞对IFN-I的关键刺激。它们被病毒感染,从而在邻近细胞中产生一种固有的细胞抗病毒状态,以对抗感染。然而,长期IFN-I信号通过抑制抑制免疫增强的抑制剂而导致免疫功能障碍[2,3]。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
"The Effect of Tissue Organization and Homeostasis on Inflammatory Cytoskeletal Signaling in Cancer"
Tissue organization and homeostasis are based on a set of circuits that include inflammatory signaling that regulates the tissue environment. Imbalance of these connections may lead to inflammatory diseases and suppression of the immune system, as occurs in chronic viral infections and cancer [1]. With interferon type I (IFN-Is) as key stimuli IFN-I are produced by virus-infected cells to create an inherent cellular antiviral status in neighboring cells to eliminate infection. However, long-term IFN-I signaling leads to impaired immune function by inducing suppressive agents that impair immunity to promote tissue organization and homeostasis [2]. Imbalance of these connections may lead to inflammatory diseases and immunosuppression, as occurs in chronic viral infections and cancer, with interferon type I (IFN-Is) as key stimuli of IFN-I by cells. They become infected with the virus to create an inherent cellular antiviral status in neighboring cells to fight infection. However, long-term IFN-I signaling leads to immune dysfunction by inhibiting suppressive agents that inhibit immune enhancement [2,3].
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