血浆和尿液中可溶性MICB解释了青少年发病系统性红斑狼疮患者NKG2D+CD4 T细胞的群体扩增。

免疫学期刊(英文) Pub Date : 2017-03-01 Epub Date: 2017-03-29 DOI:10.4236/oji.2017.71001
Satoru Hamada, Andrea Caballero-Benitez, Kate L Duran, Anne M Stevens, Thomas Spies, Veronika Groh
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引用次数: 9

摘要

异常的NKG2D配体表达与包括系统性红斑狼疮(SLE)在内的各种自身炎症性疾病的发生和维持有关。本研究的目的是确定提供NKG2D配体的细胞背景,以刺激免疫抑制性NKG2D+CD4 T细胞亚群,该亚群与调节青少年发病的SLE疾病活动有关。虽然之前对健康个体的NKG2D+CD4 T细胞的观察表明,外周B细胞和髓细胞区室可能是NKG2DL存在增强的部位,但我们没有发现证据表明在青少年发病的SLE B细胞和单核细胞中NKG2DL阳性增加与疾病相关。然而,通过ELISA检测,青少年SLE患者血浆和匹配的尿液样本中NKG2D配体MICA和MICB的可溶性形式呈阳性,这表明肾脏和/或外周血可能构成NKG2DL阳性微环境,驱动该疾病中NKG2D+CD4 T细胞群扩增。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Soluble MICB in Plasma and Urine Explains Population Expansions of NKG2D<sup>+</sup>CD4 T Cells Inpatients with Juvenile-Onset Systemic Lupus Erythematosus.

Soluble MICB in Plasma and Urine Explains Population Expansions of NKG2D<sup>+</sup>CD4 T Cells Inpatients with Juvenile-Onset Systemic Lupus Erythematosus.

Soluble MICB in Plasma and Urine Explains Population Expansions of NKG2D<sup>+</sup>CD4 T Cells Inpatients with Juvenile-Onset Systemic Lupus Erythematosus.

Soluble MICB in Plasma and Urine Explains Population Expansions of NKG2D+CD4 T Cells Inpatients with Juvenile-Onset Systemic Lupus Erythematosus.

Abnormal NKG2D ligand expression has been implicated in the initiation and maintenance of various auto-inflammatory disorders including systemic lupus erythematosus (SLE). This study's goal was to identify the cellular contexts providing NKG2D ligands for stimulation of the immunosuppressive NKG2D+CD4 T cell subset that has been implicated in modulating juvenile-onset SLE disease activity. Although previous observations with NKG2D+CD4 T cells in healthy individuals pointed towards peripheral B cell and myeloid cell compartments as possible sites of enhanced NKG2DL presence, we found no evidence for a disease-associated increase of NKG2DL-positivity among juvenile-onset SLE B cells and monocytes. However, juvenile-onset SLE patient plasma and matched urine samples were positive by ELISA for the soluble form of the NKG2D ligands MICA and MICB, suggesting that kidney and/or peripheral blood may constitute the NKG2DL positive microenvironments driving NKG2D+CD4 T cell population expansions in this disease.

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