利用单核细胞动力学治疗多发性硬化症来自实验模型研究的见解。

IF 4.1 Q2 IMMUNOLOGY
Immunotherapy advances Pub Date : 2025-04-20 eCollection Date: 2025-01-01 DOI:10.1093/immadv/ltaf003
Aqsa Bibi, Zhenjiang Yu, Lv Cui, Guiwen Yang
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引用次数: 0

摘要

单核细胞是先天免疫系统对感染或损伤反应的核心。在小鼠中,这些细胞被分为不同的亚群:经典单核细胞,由Ly6C表达升高(Ly6Chi)定义,中间单核细胞(Ly6Cint),以及非经典炎性单核细胞,以低Ly6C表达为特征(Ly6Clow)。募集到组织中的单核细胞分化为巨噬细胞,巨噬细胞可以促炎或抗炎,从而影响疾病的过程和结果。经典单核细胞的主要功能是介导促炎反应,而非经典单核细胞则与修复和抗炎过程有关,在血管腔中巡逻。越来越多的证据强调单核细胞在多发性硬化症(MS)中的重要性,多发性硬化症是一种中枢神经系统(CNS)的自身免疫性和神经退行性疾病。最近的研究表明,先天免疫系统的调节,特别是Ly6Chi单核细胞向Ly6Clow单核细胞的转变,是治疗神经退行性疾病(如阿尔茨海默氏症和多发性硬化症)的有效策略。这种转变对于将免疫反应从炎症转变为组织修复和炎症消退至关重要。强调单核细胞的可塑性及其作为多发性硬化症靶点的潜力。这篇综述与以往的研究不同之处在于,它只关注多发性硬化症的动物模型,这些模型要么直接干扰或研究单核细胞,要么治疗方法通过单核细胞介导其保护作用。这些细节允许在MS背景下对单核细胞动力学有一个微妙的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Harnessing monocyte dynamics for treatment of multiple sclerosis; insights from experimental model studies.

Monocytes are central to the innate immune system's response to infection or injury. In murine, these cells are classified into distinct subsets: classical monocytes, defined by elevated Ly6C expression (Ly6Chi), intermediate monocytes (Ly6Cint), and non-classical inflammatory monocytes, characterized by low Ly6C expression (Ly6Clow). Monocytes recruited to tissues differentiate into macrophages, which can be pro-inflammatory or anti-inflammatory, thereby influencing disease processes and outcomes. The principal function of classical monocytes is the mediation of pro-inflammatory reactions, whereas non-classical monocytes are associated with repair and anti-inflammatory processes, patrolling the lumen of the vessels. Growing evidence highlights the importance of monocytes in multiple sclerosis (MS), an autoimmune and neurodegenerative disease of the central nervous system (CNS). Recent studies indicate that modulation of the innate immune system, focusing specifically on the shift from Ly6Chi to Ly6Clow monocytes, is an effective therapeutic strategy for neurodegenerative diseases, such as Alzheimer's and MS. This transition is crucial for switching the immune response from inflammation to tissue repair and inflammation resolution, emphasizing the plasticity of monocytes and their potential as targets in MS. This review differs from prior studies in that it focuses solely on animal models of MS, which either directly perturb or study monocytes, or where therapeutic approaches mediate their protective effects through monocytes. Such details permit a subtle comprehension of monocyte dynamics in the context of MS.

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