The CD14++CD16+ monocyte subset is expanded and controls Th1 cell development in Graves’ disease
The CD14++CD16+ monocyte subset is expanded and controls Th1 cell development in Graves’ disease
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CD14 CD16 单核细胞亚群扩增并控制 Graves 病中 Th1 细胞的发育
DOI：
10.1016/j.clim.2022.109160
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发表时间：
2022
影响因子：
8.6
通讯作者：
Yin Qinglei
中科院分区：
文献类型：
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作者：
Yin Qinglei
最近发现了三种不同的单核细胞亚群，即CD14++CD16−(经典)、CD14++CD16+(中间)和CD14+CD16+(非经典)单核细胞。新的证据表明，在自身免疫性疾病中，中间单核细胞或CD16+(中间和非经典)单核细胞水平升高。然而，关于每个单核细胞亚群在Graves病(GD)发病机制中的作用的研究还很缺乏。我们的目的是研究这些亚群的临床意义及其在GD发病机制中的潜在作用。在GD患者中，CD14++CD16+单核细胞比其他单核细胞亚群表现出更多的激活状态。GD患者外周血中CD14++CD16+单核细胞比例升高，CD14++CD16+单核细胞比例下降，且CD14++CD16+单核细胞比例与GD临床参数呈正相关。随访分析显示，治疗后CD_(14+)+CD_(16)单核细胞百分率升高，CD_(14+)CD_(16+)−百分率下降。我们发现CD14+CD16+GD单核细胞能促进干扰素-γ+CD4+细胞的增殖。Th1极化细胞因子IL-12在与患者CD14+CD16+单核细胞和CD4+T细胞直接接触后分泌，负责干扰素-γ+CD4+细胞的发育。我们的结果提示CD14++CD16+单核细胞参与了GD的发病过程，并且CD14++CD16+单核细胞在GD潜在致病Th反应的产生中起着关键作用。
Three different subsets of circulating human monocytes, CD14++CD16− (classical), CD14++CD16+ (intermediate), and CD14+CD16+ (non-classical) monocytes, have been recently identified. New evidence suggests that .levels of intermediate monocytes or CD16+ (intermediate and non-classical) monocytes are increased in autoimmune diseases. However, studies regarding the role of each monocyte subset in the pathogenesis of Graves’ .disease (GD) are lacking. We aimed to investigate the clinical implications of these subsets and their potential .role in GD pathogenesis. CD14++CD16+ monocytes showed a more activated state in GD patients than other .monocyte subpopulations. An increased proportion of circulating CD14++CD16+ monocytes and a decreased .proportion of circulating CD14++CD16− monocytes in GD patients were detected, and CD14++CD16+ monocyte .frequencies were positively correlated with GD clinical parameters. Additionally, a follow-up analysis indicated .that the CD14++CD16− monocyte percentage increased and the CD14++CD16+ monocyte percentage decreased .post-treatment. We found that CD14++CD16+ GD monocytes promoted the expansion of IFN-γ+CD4+ cells. The .Th1-polarizing cytokine IL-12, secreted after direct contact with patient CD14++CD16+ monocytes and CD4+ T .cells, was responsible for IFN-γ+CD4+ cell development. Our results suggest that CD14++CD16+ monocytes are .involved in GD pathogenesis and the critical role of CD14++CD16+ monocytes in the generation of potentially .pathogenic Th responses in GD.