Modulation of IL-4/IL-13 cytokine signaling in the context of allergic disease.
Modulation of IL-4/IL-13 cytokine signaling in the context of allergic disease.
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过敏性疾病背景下IL-4/IL-13细胞因子信号传导的调节。
DOI：
10.1016/j.jaci.2022.06.012
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发表时间：
2022-08
影响因子：
14.2
通讯作者：
Lewkowich, Ian P.
中科院分区：
文献类型：
--
作者：
Shankar, Archana;McAlees, Jaclyn W.;Lewkowich, Ian P.
CD 4辅助性T细胞2（Th 2）的异常活化和Th 2细胞因子如白细胞介素（IL）-4和IL-13的过度产生与变应性疾病的发病机制有关。通常，IL-4和IL-13利用JAK-STAT信号传导途径诱导炎症基因表达和与许多过敏性疾病中的疾病病理学相关的效应子功能。然而，越来越清楚的是，由IL-4/IL-13激活的JAK/STAT途径本身可以在其他细胞内信号传导程序的存在下被调节，从而改变IL-4/IL-13信号传导的整体音调和/或幅度。除了直接激活经典JAK-STAT途径外，IL-4和IL-13还通过激活额外的信号级联诱导促炎基因表达和效应子功能。这些替代信号级联有助于IL-4/IL-13相关的细胞和分子应答的几个特定方面。对IL-4/IL-13信号通路的更全面的理解，包括非经典信号通路被激活的精确条件，以及这些通路对细胞和宿主水平反应的影响，将使我们能够更好地设计针对特定病理结果的药物，或为治疗不常见疾病的内在型定制治疗方法。
Aberrant activation of CD4 T helper 2 (Th2) cells and excessive production of Th2 cytokines like interleukin (IL)-4 and IL-13 have been implicated in the pathogenesis of allergic diseases. Generally, IL-4 and IL-13 utilize JAK-STAT signaling pathways for induction of inflammatory gene expression and the effector functions associated with disease pathology in many allergic diseases. However, it is increasingly clear that JAK/STAT pathways activated by IL-4/IL-13 can themselves be modulated in the presence of other intracellular signaling programs, thereby changing the overall tone and/or magnitude of IL-4/IL-13 signaling. Apart from direct activation of the canonical JAK-STAT pathways, IL-4 and IL-13 also induce pro-inflammatory gene expression and effector functions through activation of additional signaling cascades. These alternative signaling cascades contribute to several specific aspects of IL-4/IL-13-associated cellular and molecular responses. A more complete understanding of IL-4/IL-13 signaling pathways, including the precise conditions under which non-canonical signaling pathways are activated, and the impact of these pathways on cellular and host level responses, will better allow us to design agents that target specific pathological outcomes, or tailor therapies for the treatment of uncommon disease endotypes.
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