Yu Yang, Qiao Mingbiao, Liu Jinbo, Guo Yuanbiao, Sun Yueshan
Department of Laboratory Medicine, the Affiliated Hospital of Southwest Medical University, Luzhou, China.
Xindu District People's Hospital of Chengdu, Chengdu, China.
Clin Exp Med. 2025 Jun 4;25(1):187. doi: 10.1007/s10238-025-01695-y.
Autophagy, a critical cellular process for maintaining homeostasis, involves the degradation and recycling of cellular components through double-membraned vesicles that are transported to lysosomes. This mechanism plays a pivotal role in the immune system by influencing cell fate decisions and functional differentiation. Emerging evidence indicates that autophagy significantly impacts the differentiation and function of T cells and group 3 innate lymphoid cell (ILC3), which are the primary producers of Interleukin-22 (IL-22). IL-22, a key cytokine involved in modulating immune responses and maintaining tissue integrity, is particularly important in combating inflammatory diseases, infections, and cancer. It exerts its effects through a signaling pathway that involves the IL-22R1 and IL-10R2 receptors. Studies have demonstrated that IL-22 can promote autophagy by activating the AMPK pathway and that its intervention can upregulate the expression of autophagy-related genes, underscoring its significant role in the regulation of autophagy. These findings reveal a complex relationship and bidirectional relationship between autophagy and IL-22, highlighting their multifaceted interactions under both physiological and pathological conditions. This review aims to provide a detailed exploration of the dynamic interplay between autophagy and IL-22, with a focus on their mutual regulatory mechanisms, functional significance, and potential for therapeutic interventions. By performing a comprehensive analysis, we sought to clarify the intricate cross talk between autophagy and IL-22, thereby advancing our understanding of their roles in cellular and immune homeostasis and their potential as targets for clinical interventions.
自噬是维持体内平衡的关键细胞过程，涉及通过运输到溶酶体的双膜囊泡对细胞成分进行降解和循环利用。该机制通过影响细胞命运决定和功能分化在免疫系统中发挥关键作用。新出现的证据表明，自噬对T细胞和3型固有淋巴细胞（ILC3）的分化和功能有显著影响，而ILC3是白细胞介素-22（IL-22）的主要产生者。IL-22是参与调节免疫反应和维持组织完整性的关键细胞因子，在对抗炎症性疾病、感染和癌症方面尤为重要。它通过涉及IL-22R1和IL-10R2受体的信号通路发挥作用。研究表明，IL-22可通过激活AMPK通路促进自噬，其干预可上调自噬相关基因的表达，突显了其在自噬调节中的重要作用。这些发现揭示了自噬与IL-22之间复杂的双向关系，突出了它们在生理和病理条件下多方面的相互作用。本综述旨在详细探讨自噬与IL-22之间的动态相互作用，重点关注它们的相互调节机制、功能意义以及治疗干预潜力。通过进行全面分析，我们试图阐明自噬与IL-22之间复杂的相互作用，从而增进我们对它们在细胞和免疫稳态中的作用以及作为临床干预靶点潜力的理解。
