Mohammad Zainab B, Yudin Samantha C Y, Goldberg Benjamin J, Serra Kursti L, Klegeris Andis
Laboratory of Cellular and Molecular Pharmacology, Department of Biology, University of British Columbia Okanagan Campus, Kelowna, BC, V1V 1V7, Canada.
Rev Neurosci. 2024 Sep 3;36(1):91-117. doi: 10.1515/revneuro-2024-0081. Print 2025 Jan 29.
Effective communication between different cell types is essential for brain health, and dysregulation of this process leads to neuropathologies. Brain glial cells, including microglia and astrocytes, orchestrate immune defense and neuroimmune responses under pathological conditions during which interglial communication is indispensable. Our appreciation of the complexity of these processes is rapidly increasing due to recent advances in molecular biology techniques, which have identified numerous phenotypic states of both microglia and astrocytes. This review focuses on microglia-to-astrocyte communication facilitated by secreted neuroimmune modulators. The combinations of interleukin (IL)-1α, tumor necrosis factor (TNF), plus complement component C1q as well as IL-1β plus TNF are already well-established microglia-derived stimuli that induce reactive phenotypes in astrocytes. However, given the large number of inflammatory mediators secreted by microglia and the rapidly increasing number of distinct functional states recognized in astrocytes, it can be hypothesized that many more intercellular signaling molecules exist. This review identifies the following group of cytokines and gliotransmitters that, while not established as interglial mediators yet, are known to be released by microglia and elicit functional responses in astrocytes: IL-10, IL-12, IL-18, transforming growth factor (TGF)-β, interferon (IFN)-γ, C-C motif chemokine ligand (CCL)5, adenosine triphosphate (ATP), l-glutamate, and prostaglandin E2 (PGE2). The review of molecular mechanisms engaged by these mediators reveals complex, partially overlapping signaling pathways implicated in numerous neuropathologies. Additionally, lack of human-specific studies is identified as a significant knowledge gap. Further research on microglia-to-astrocyte communication is warranted, as it could discover novel interglial signaling-targeted therapies for diverse neurological disorders.
不同细胞类型之间的有效沟通对大脑健康至关重要,而这一过程的失调会导致神经病理学变化。脑胶质细胞,包括小胶质细胞和星形胶质细胞,在病理条件下协调免疫防御和神经免疫反应,在此期间胶质细胞间的通讯不可或缺。由于分子生物学技术的最新进展,我们对这些过程复杂性的认识正在迅速增加,这些进展已经确定了小胶质细胞和星形胶质细胞的众多表型状态。本综述聚焦于由分泌的神经免疫调节剂促进的小胶质细胞与星形胶质细胞之间的通讯。白细胞介素(IL)-1α、肿瘤坏死因子(TNF)加上补体成分C1q以及IL-1β加上TNF的组合,已经是公认的源自小胶质细胞的刺激物,可诱导星形胶质细胞产生反应性表型。然而,鉴于小胶质细胞分泌的大量炎症介质以及在星形胶质细胞中识别出的不同功能状态数量迅速增加,可以推测存在更多的细胞间信号分子。本综述确定了以下一组细胞因子和神经递质,虽然它们尚未被确定为胶质细胞间的介质,但已知由小胶质细胞释放并在星形胶质细胞中引发功能反应:IL-10、IL-12、IL-18、转化生长因子(TGF)-β、干扰素(IFN)-γ、C-C基序趋化因子配体(CCL)5、三磷酸腺苷(ATP)、L-谷氨酸和前列腺素E2(PGE2)。对这些介质所涉及的分子机制的综述揭示了与众多神经病理学相关的复杂、部分重叠的信号通路。此外,缺乏针对人类的研究被确定为一个重大的知识空白。有必要进一步研究小胶质细胞与星形胶质细胞之间的通讯,因为这可能会发现针对多种神经系统疾病的新型胶质细胞间信号靶向疗法。