Hu Di, Yang Zisha, Zhang Jun-Ai, Liu Ganbin, Pi Jiang, Xu Junfa, Wang Yan, Zhao Yi
Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics The First Dongguan Affiliated Hospital, Guangdong Medical University Dongguan Guangdong China.
Institute of Laboratory Medicine, School of Medical Technology Guangdong Medical University Dongguan Guangdong China.
FASEB Bioadv. 2024 Dec 25;7(1):e1484. doi: 10.1096/fba.2024-00166. eCollection 2025 Jan.
Copper is a vital trace element crucial for mediating interactions between and macrophages. Within these immune cells, copper modulates oxidative stress responses and signaling pathways, enhancing macrophage immune functions and facilitating clearance. Conversely, copper may promote escape from macrophages through various mechanisms: inhibiting macrophage activity, diminishing phagocytic and bactericidal capacities, and supporting survival and proliferation. This paradox has intensified research focus on the regulatory role of copper in immune cell-pathogen interactions. Interactions among metal ions can affect concentration, distribution, and activity within an organism. In this review, we have elucidated the role of copper in these interactions, focusing on the mechanisms by which this metal influences both the immune defense mechanisms of macrophages and the survival strategies of . The findings suggest that manipulating copper levels could enhance macrophage bactericidal functions and potentially limit resistance. Therefore, elucidating the regulatory role of copper is pivotal for advancing our understanding of metal homeostasis in immune cell-pathogen dynamics and TB pathogenesis. Furthermore, we recommend further investigation into the role of copper in TB pathogenesis to advance tuberculosis diagnosis and treatment and gain comprehensive insights into metal homeostasis in infectious disease contexts.
铜是一种至关重要的微量元素，对于介导[具体内容缺失]与巨噬细胞之间的相互作用至关重要。在这些免疫细胞中，铜调节氧化应激反应和信号通路，增强巨噬细胞免疫功能并促进[具体内容缺失]清除。相反，铜可能通过多种机制促进[具体内容缺失]从巨噬细胞中逃逸：抑制巨噬细胞活性、降低吞噬和杀菌能力以及支持[具体内容缺失]存活和增殖。这种矛盾加剧了对铜在免疫细胞 - 病原体相互作用中调节作用的研究关注。金属离子之间的相互作用会影响生物体内[具体内容缺失]的浓度、分布和活性。在本综述中，我们阐明了铜在这些相互作用中的作用，重点关注这种金属影响巨噬细胞免疫防御机制和[具体内容缺失]生存策略的机制。研究结果表明，控制铜水平可以增强巨噬细胞杀菌功能并可能限制[具体内容缺失]耐药性。因此，阐明铜的调节作用对于推进我们对免疫细胞 - 病原体动态和结核病发病机制中金属稳态的理解至关重要。此外，我们建议进一步研究铜在结核病发病机制中的作用，以推进结核病诊断和治疗，并全面了解传染病背景下的金属稳态。
