Aberrant activation of CD4 T_H2 cells and excessive production of T_H2 cytokines such as IL-4 and IL-13 have been implicated in the pathogenesis of allergic diseases. Generally, IL-4 and IL-13 utilize Janus kinase (JAK)/signal transducer and activator of transcription (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 canonic JAK/STAT pathways, IL-4 and IL-13 also induce proinflammatory 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 noncanonic 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 pathologic outcomes or tailor therapies for the treatment of uncommon disease endotypes.

CD4 T _H 2 细胞的异常激活和T _H 2 细胞因子（例如IL-4 和IL-13）的过量产生与过敏性疾病的发病机制有关。一般来说，IL-4和IL-13利用Janus激酶(JAK)/信号转导器和转录激活子(STAT)信号通路来诱导炎症基因表达以及与许多过敏性疾病的疾病病理学相关的效应器功能。然而，越来越清楚的是，IL-4/IL-13 激活的 JAK/STAT 通路本身可以在其他细胞内信号传导程序存在的情况下进行调节，从而改变 IL-4/IL-13 的整体音调和/或强度发信号。除了直接激活典型的 JAK/STAT 通路外，IL-4 和 IL-13 还通过激活其他信号级联来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 相关细胞和分子反应的几个特定方面。更全面地了解 IL-4/IL-13 信号通路，包括非经典信号通路激活的精确条件，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出以下药物：针对特定的病理结果或针对罕见疾病内型的治疗定制疗法。