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CC Chemokine Ligand 25 Enhances Resistance to Apoptosis in CD4⁺ T Cells from Patients with T-Cell Lineage Acute and Chronic Lymphocytic Leukemia by Means of Livin Activation

¹ Department of Immunology, and Laboratory of Allergy and Clinical Immunology, Institute of Allergy and Immune-related Diseases and Center for Medical Research, Wuhan University School of Medicine, Wuhan; ² The State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Science, Shanghai; ³ Department of Immunology, College of Basic Medical Sciences, Anhui Medical University, Hefei; ⁴ Department of Hematology, The Affiliated University Hospital, Anhui Medical University, Hefei; ⁵ Department of Hematology, The First and Second Affiliated University Hospital, Wuhan University, Wuhan; and ⁶ Department of Hematology, The Provincial Hospital of Anhui, Hefei, Peoples Republic of China

We investigated CD4 and CD8 double-positive thymocytes, CD4⁺ T cells from typical patients with T-cell lineage acute lymphocytic leukemia (T-ALL) and T cell lineage chronic lymphocytic leukemia (T-CLL), and MOLT4 T cells in terms of CC chemokine ligand 25 (CCL25) functions of induction of resistance to tumor necrosis factor (TNF-)–mediated apoptosis. We found that CCL25 selectively enhanced resistance to TNF-–mediated apoptosis in T-ALL and T-CLL CD4⁺ T cells as well as in MOLT4 T cells, but CD4 and CD8 double-positive thymocytes did not. One member protein of the inhibitor of apoptosis protein (IAP) family, Livin, was selectively expressed in the malignant cells at higher levels, particularly in T-ALL CD4⁺ T cells, in comparison with the expression in CD4 and CD8 double-positive thymocytes. After stimulation with CCL25 and apoptotic induction with TNF-, the expression levels of Livin in these malignant cells were significantly increased. CCL25/thymus-expressed chemokine (TECK), by means of CC chemokine receptor 9 (CCR9) ligation, selectively activated Livin to enhance resistance to TNF-–mediated apoptosis in c-jun-NH₂-kinase 1 (JNK1) kinase-dependent manner. These findings suggested differential functions of CCR9/CCL25 in distinct types of cells. CD4 and CD8 double-positive thymocytes used CCR9/CCL25 for migration, homing, development, maturation, selection, cell homeostasis, whereas malignant cells, particularly T-ALL CD4⁺ T cells, used CCR9/CCL25 for infiltration, resistance to apoptosis, and inappropriate proliferation.

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