Publication: Mechanism of paroxysmal nocturnal hemoglobinuria clonal dominance: Possible roles of different apoptosis and CD8+ lymphocytes in the selection of paroxysmal nocturnal hemoglobinuria clones
Issued Date
2013-04-02
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16583876
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2-s2.0-84875451921
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Mahidol University
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SCOPUS
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Hematology/ Oncology and Stem Cell Therapy. Vol.5, No.3 (2013), 138-145
Suggested Citation
Rajita Kunyaboon, Wanchai Wanachiwanawin, Pratya U-Yaowalak, Anchalee Thedsawad, Orathai Taka Mechanism of paroxysmal nocturnal hemoglobinuria clonal dominance: Possible roles of different apoptosis and CD8+ lymphocytes in the selection of paroxysmal nocturnal hemoglobinuria clones. Hematology/ Oncology and Stem Cell Therapy. Vol.5, No.3 (2013), 138-145. doi:10.5144/1658-3876.2012.138 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/32400
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Title
Mechanism of paroxysmal nocturnal hemoglobinuria clonal dominance: Possible roles of different apoptosis and CD8+ lymphocytes in the selection of paroxysmal nocturnal hemoglobinuria clones
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Abstract
Background and objectives: Paroxysmal nocturnal hemoglobinuria (PNH), a clonal hematopoietic stem cell disorder, manifests when the PNH clone populates in the hematopoietic compartment. We explored the roles of different apoptosis of GPI+ and GPI- (glycosylphosphatidylinositol) cells and CD8+ lymphocytes in a selection of PNH clones. Patients and Methods: Granulocytes from PNH patients and normal controls were subjected to an apoptosis assay using annexin V. Hematopoietic cell in semisolid media were cultured with or without CD8+ lymphocytes. Results: In PNH, CD59+ granulocytes exhibited more apoptosis than their CD59- counterparts, after 0 or 4 hours in liquid growth culture system (mean [standard error of mean]: 2.1 (0.5) vs 1.2 (0.2), P=.01 at 0 hour and 3.4 [0.7] vs 1.8 [0.3], P=.03 at 4 hour, respectively). The presence of mononuclear cells (MNCs) rendered a greater difference in apoptosis. The percentages of apoptotic CD59+ granulocytes measured at 4 hours with or without MNC fraction were correlated with the sizes of PNH clones (r=0.633, P=.011; and r=0.648, P=.009; respectively). The autologous CD8+ lymphocytes inhibited CFU-GM and BFU-E colony formation in PNH patients when compared with normal controls (mean [SEM] of percentages of inhibition: 61.7 (10.4) vs 11.9 (2.0), P=.008 for CFU-GM and 26.1 (6.9) vs 4.9 (1.0), P=.037 for BFU-E). Conclusions: Increased apoptosis of GPI+ blood cells is likely to be responsible in selection and expansion of PNH clones. MNCs or possibly CD8+ lymphocytes may play a role in this phenomenon.