NKG2D公司
FOXP3型
白细胞介素2受体
关贸总协定3
白细胞介素21
关节炎
白细胞介素12
免疫学
化学
T细胞
细胞生物学
细胞毒性T细胞
分子生物学
内科学
生物
医学
免疫系统
体外
转录因子
生物化学
基因
作者
Juan Zhou,Junyan Wang,Linlin Tao,Mingyue Liu,Xuemei Tang,Xiaoping Zhu
标识
DOI:10.1016/j.clim.2023.109780
摘要
NKG2D provides a costimulatory signal for activation of CD4+ T cells. We explored its role in interactions of CD4+ T cells and dendritic cells (DCs) in juvenile idiopathic arthritis (JIA) patients by using NKG2D genetically modified CD4+ T cells. We found active JIA patients had significantly higher content of CD4 + NKG2D+ T cells than healthy controls. Expression of NKG2D on CD4+ T cells, and MICA and MICB on DCs were significantly greater in articular JIA than systemic JIA. NKG2D induced IL- 12 and suppressed IL-10 and TGF-β from CD4+ T cells, increased IFN-γ + CD4+ T and IL-17+ CD4+ T cells, RORc and T-bet, but reduced CD25+ Foxp3+ CD4+ T cells, IL-4+ CD4+ T cells, Foxp3, and GATA3 in JIA patients. NKG2D decreased IL-10 and increased CD83, MICA, and MICB of DCs in JIA and controls. So NKG2D regulates differentiation of CD4+ T cells directly and the maturation of DCs indirectly.
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