CD16(+) Monocyte Subset Was Enriched and Functionally Exacerbated in Driving T-Cell Activation and B-Cell Response in Systemic Lupus Erythematosus.
CD16(+) Monocyte Subset Was Enriched and Functionally Exacerbated in Driving T-Cell Activation and B-Cell Response in Systemic Lupus Erythematosus.
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CD 16( ) 单核细胞亚群在系统性红斑狼疮中驱动 T 细胞激活和 B 细胞反应的过程中得到丰富且功能增强
DOI:
10.3389/fimmu.2016.00512
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发表时间:
2016
影响因子:
7.3
通讯作者:
Su Y
中科院分区:
文献类型:
--
作者:
Zhu H;Hu F;Sun X;Zhang X;Zhu L;Liu X;Li X;Xu L;Shi L;Gan Y;Su Y
The roles that CD16+ monocyte subset plays in T-cell activation and B-cell response have not been well studied in systemic lupus erythematosus (SLE). The present study aimed to investigate the distribution of CD16+ monocyte subsets in SLE and explore their possible roles in T-cell activation and B-cell differentiation. The frequencies of monocyte subsets in the peripheral blood of healthy controls (HCs) and patients with SLE were determined by flow cytometry. Monocyte subsets were sorted and cocultured with CD4+ T cells and CD19+ B cells. Then, T and B cells were collected for different subset detection, while the supernatants were collected for immunoglobulin G, IgA, and IgM or interferon-γ and interleukin-17A detection by enzyme-linked immunosorbent assay. Our results showed that CD16+ monocytes exhibited a proinflammatory phenotype with elevated CD80, CD86, HLA-DR, and CX3CR1 expression on the cell surface. It’s further demonstrated that CD16+ monocytes from patients and HCs shared different cell-surface marker profiles. The CD16+ subset was enriched in SLE and had an exacerbated capacity to promote CD4+ T cell polarization into a Th17 phenotype. Also, CD16+ monocytes had enhanced impacts on CD19+ B cells to differentiate into plasma B cells and regulatory B cells with more Ig production. This study demonstrated that CD16+ monocytes, characterized by different cell-surface marker profiles, were enriched and played a critical role in driving the pathogenic T- and B-cell responses in patients with SLE.
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影响因子:
4.9
作者:
Hilliard BA;Zizzo G;Ulas M;Linan MK;Schreiter J;Cohen PL
通讯作者:
Cohen PL
影响因子:
13.6
作者:
Crispín JC;Liossis SN;Kis-Toth K;Lieberman LA;Kyttaris VC;Juang YT;Tsokos GC
通讯作者:
Tsokos GC
影响因子:
5.5
作者:
Kim, Woong-Ki;Sun, Yue;Williams, Kenneth
通讯作者:
Williams, Kenneth
影响因子:
3.2
作者:
Castano, Diana;Garcia, Luis F.;Rojas, Mauricio
通讯作者:
Rojas, Mauricio
影响因子:
13.3
作者:
Burbano, C.;Vasquez, G.;Rojas, M.
通讯作者:
Rojas, M.