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首页> 外文期刊>Diseases of the esophagus: official journal of the International Society for Diseases of the Esophagus >Inverse correlation between NKG2D expression on CD8+ T cells and the frequency of CD4+CD25+ regulatory T cells in patients with esophageal cancer.
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Inverse correlation between NKG2D expression on CD8+ T cells and the frequency of CD4+CD25+ regulatory T cells in patients with esophageal cancer.

机译:食管癌患者CD8 + T细胞上NKG2D表达与CD4 + CD25 +调节性T细胞频率呈负相关。

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Although malignant diseases are known to be associated with immune suppression, detailed mechanisms of this phenomenon are still unknown. NKG2D is an activating cell surface receptor expressed by natural killer (NK) cells and CD8+ T cells, and it has been reported that NKG2D engagement is extremely important for T cell activation. In the current study, NKG2D expression on CD8+ T cells and the frequency of CD4+ CD25+ regulatory T (Treg) cells were determined by multicolor flow cytometry to investigate one of the mechanisms responsible for immune evasion in esophageal cancer patients. NKG2D expression on CD8+ T lymphocytes in esophageal cancer patients was significantly lower than in those of normal controls. NKG2D expression in T3/T4 esophageal cancer was significantly lower than that in T1/T2 esophageal cancer. CD8+ T cells from patients with lymph node metastasis expressed significantly lower NKG2D than those without lymph node metastasis. Moreover, significantly lower NKG2D expression was observed instage III/IV cancer in comparison with stage I/II. The frequency of CD4+CD25+ Treg cells in esophageal cancer patients was significantly higher than those in normal controls. NKG2D expression on CD8+ T cells was significantly inversely correlated with the frequency of CD4+CD25+ Treg cells in esophageal cancer patients. Our data indicates that decreased NKG2D expression on CD8+ T cells is correlated with disease severity. Decreased NKG2D expression and an increase in Treg cells may be one of the key mechanisms responsible for immune evasion in esophageal cancer.
机译:尽管已知恶性疾病与免疫抑制有关,但这种现象的详细机制仍然未知。 NKG2D是天然杀伤(NK)细胞和CD8 + T细胞表达的活化细胞表面受体,据报道,NKG2D的参与对T细胞活化极为重要。在本研究中,通过多色流式细胞术确定了CD8 + T细胞上NKG2D的表达以及CD4 + CD25 +调节性T(Treg)细胞的频率,以研究导致食管癌患者免疫逃逸的机制之一。食管癌患者CD8 + T淋巴细胞的NKG2D表达明显低于正常对照组。在T3 / T4食管癌中NKG2D表达明显低于在T1 / T2食管癌中。淋巴结转移患者的CD8 + T细胞表达的NKG2D明显低于无淋巴结转移患者。此外,与I / II期相比,III / IV期癌症中NKG2D表达明显降低。食管癌患者中CD4 + CD25 + Treg细胞的频率显着高于正常对照组。在食管癌患者中,CD8 + T细胞上的NKG2D表达与CD4 + CD25 + Treg细胞的频率显着负相关。我们的数据表明,CD8 + T细胞上NKG2D表达的降低与疾病的严重程度相关。 NKG2D表达减少和Treg细胞增加可能是导致食管癌免疫逃逸的关键机制之一。

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