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首页> 外文期刊>Oncogene >Selectively frequent expression of CXCR5 enhances resistance to apoptosis in CD8+CD34+ T cells from patients with T-cell-lineage acute lymphocytic leukemia
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Selectively frequent expression of CXCR5 enhances resistance to apoptosis in CD8+CD34+ T cells from patients with T-cell-lineage acute lymphocytic leukemia

机译：CXCR5的频繁表达增强了来自T细胞谱系急性淋巴细胞白血病患者的CD8 + CD34 + T细胞对凋亡的抗性

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We investigated CD4+CD34+, CD8+CD34+, CD4+CD34-, and CD8+CD34- T cells from cord blood and from typical patients with T-cell-lineage acute lymphocytic leukemia and T-cell-lineage chronic lymphocytic leukemia in terms of expression and functions of CXCR5/CXCL13. We found that CXCR5 was selectively frequently expressed on T-cell-lineage acute (chronic) lymphocytic leukemia (T-ALL) CD8+CD34+ T cells, but not on T-ALL CD4+CD34+, CD4+CD34-, and CD8+CD34- T cells. CXCR5 was rarely expressed on all types of CD34+ and CD34- CB or T-CLL T cells. CXCL13/B cells attracting chemokine 1 induced significant resistance to TNF--mediated apoptosis in T-ALL CD8+CD34+ T cells, instead of induction of chemotactic and adhesive responsiveness. A proliferation-inducing ligand expression in T-ALL CD8+CD34+ T cells was upregulated by CXCL13/BCA-1 (B-cell attracting chemokine 1). The CXCR5/CXCL13 pair by means of activation of APRIL (A proliferation-inducing ligand) induced resistance to apoptosis in T-ALL CD8+CD34+ T cells in livin-dependent manner. In this process, cell–cell contact in culture was necessary. Based on our findings, we suggested that there were differential functions of CXCR5/CXCL13 in distinct types of cells. Normal lymphocytes, especially na?ve B and T cells, utilized CXCR5/CXCL13 for migration, homing, maturation, and cell homeostasis, as well as secondary lymphoid tissue organogenesis. Meanwhile, certain malignant cells took advantages of CXCR5/CXCL13 for infiltration, resistance to apoptosis, and inappropriate proliferation.
机译：我们研究了CD4 + CD34 +，CD8 + CD34 +，CD4 + CD34-，CD8 + CD34- T细胞和来自典型的T细胞谱系急性淋巴细胞白血病和T细胞谱系慢性淋巴细胞白血病的典型患者CXCR5 / CXCL13的表达与功能。我们发现CXCR5在T细胞谱系急性（慢性）淋巴细胞白血病（T-All）CD8 + CD34 + T细胞上选择性地经常表达，但不含T-All CD4 + CD34 +，CD4 + CD34-和CD8 + CD34 - t细胞。 CXCR5很少在所有类型的CD34 +和CD34-CB或T-CLL T细胞上表达。吸引趋化因子的CXCL13 / B细胞1在T-All CD8 + CD34 + T细胞中诱导对TNF介导的凋亡的显着抗性，而不是诱导趋化性和粘合剂反应性。通过CXCl13 / BCA-1（B细胞吸引趋化因子1）上调，诱导诱导T-所有CD8 + CD34 + T细胞中的增殖配体表达。 CXCR5 / CXCL13对通过激活4月（增殖诱导配体）诱导在Livin依赖性方式中诱导对T-all CD8 + CD34 + T细胞凋亡的抗性。在该过程中，需要培养中的细胞细胞接触。基于我们的研究结果，我们建议在不同类型的细胞中存在CXCR5 / CXCL13的差异功能。正常淋巴细胞，尤其是Naαve B和T细胞，用于迁移，归巢，成熟和细胞稳态，以及次级淋巴组织器官组织的CXCR5 / CXCL13。同时，某些恶性细胞利用CXCR5 / CXCL13进行渗透，抗细胞凋亡，不恰当的增殖。

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