Decreased CCR2 and CD62L expressions on peripheral blood classical monocytes in amyotrophic lateral sclerosis.
Decreased CCR2 and CD62L expressions on peripheral blood classical monocytes in amyotrophic lateral sclerosis.
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肌萎缩侧索硬化症患者外周血经典单核细胞 CCR2 和 CD62L 表达降低。
DOI：
10.1111/cen3.12088
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发表时间：
2014
期刊：
影响因子：
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通讯作者：
et al.
中科院分区：
文献类型：
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作者：
Cui Y;et al.
目的最近的证据表明异常激活的单核细胞系统在肌萎缩侧索硬化症 (ALS) 发病机制中的重要性。然而，每个单核细胞亚群，即 CD14+CD16− 经典单核细胞、CD14dimCD16+ 非经典单核细胞和 CD14+CD16+ 中间单核细胞在 ALS 中的作用仍然未知。我们的目的是阐明ALS中单核细胞亚群比例和每个单核细胞亚群表面标志物表达的变化。方法采集19名ALS患者和28名健康对照（HC）的血液样本。采用流式细胞仪检测三种单核细胞亚群（经典型、非经典型和中间型）中 CCR2、CX3CR1、CD64 和 CD62L 的表面表达。结果 ALS 患者 CD14+CD16− 经典单核细胞上 CCR2 和 CD62L 的百分比显着低于 HC（P=0.0012 和 P=0.0296， 分别）。每个单核细胞亚群的 CX3CR1 和 CD64 没有发现差异。中间单核细胞的百分比与修订后的 ALS 功能评定量表得分呈显着负相关（r=−0.631，P=0.0038）。结论 ALS 中存在经典炎症单核细胞上趋化和粘附相关分子的减少，进一步表明异常的先天免疫系统参与了 ALS 发病机制。
ObjectiveRecent evidence has suggested the importance of an aberrantly activated monocyte system in amyotrophic lateral sclerosis (ALS) pathogenesis. However, the roles of each monocyte subset, namely CD14+CD16− classical monocytes, CD14dimCD16+ non‐classical monocytes and CD14+CD16+ intermediate monocytes, in ALS remain unknown. We aimed to clarify the alterations in the monocyte subset proportions and the surface marker expressions on each monocyte subset in ALS.MethodsBlood samples were collected from 19 ALS patients and 28 healthy controls (HC). The surface expressions of CCR2, CX3CR1, CD64 and CD62L were measured in the three monocyte subsets (classical, non‐classical and intermediate) by flow cytometry.ResultsThe percentages of CCR2 and CD62L on CD14+CD16− classical monocytes were significantly lower in ALS patients than in HC (P=0.0012 andP=0.0296, respectively). No differences were found in CX3CR1 and CD64 on each monocyte subset. The percentage of intermediate monocytes showed a significant negative correlation with the revised ALS functional rating scale score (r= −0.631,P= 0.0038).ConclusionsReductions in chemotaxis‐ and adhesion‐related molecules on classical inflammatory monocytes are present in ALS, further suggesting the involvement of an aberrant innate immune system in ALS pathogenesis.