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- Title
Selectively frequent expression of CXCR5 enhances resistance to apoptosis in CD8<sup>+</sup>CD34<sup>+</sup> T cells from patients with T-cell-lineage acute lymphocytic leukemia.
- Authors
Qiuping, Zhang; Jie, Xiong; Youxin, Jin; Qun, Wu; Wei, Ju; Chun, Liu; Jin, Wang; Yan, Liu; Chunsong, Hu; Mingzhen, Yang; Qingping, Gao; Qun, Li; Kejian, Zhang; Zhimin, Sun; Junyan, Liu; Jinquan, Tan
- Abstract
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-a-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 naïve 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.Oncogene (2005) 24, 573-584. doi:10.1038/sj.onc.1208184 Published online 6 December 2004
- Subjects
APOPTOSIS; CELL death; LEUCOCYTOSIS; LYMPHOBLASTIC leukemia; PRELEUKEMIA; PHYSIOLOGICAL control systems; CHRONIC diseases
- Publication
Oncogene, 2005, Vol 24, Issue 4, p573
- ISSN
0950-9232
- Publication type
Article
- DOI
10.1038/sj.onc.1208184