Inhibition of interleukin-2 receptor (CD25) expression induced on T cells from children with acute lymphoblastic leukemia |
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Authors: | X.-L. Zhang Y. Komada Yan-Wen Zhou Tong-Xin Chen Haruko Sakai Eiichi Azuma Masaru Ido Minoru Sakurai |
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Affiliation: | (1) Department of Pediatrics, Mie University School of Medicine, 2-174 Edobashi, Tsu Mie 514, Japan Fax: 0592 31 5213, JP;(2) Department of Clinical Immunology, Mie University School of Medicine, Mie, Japan, JP;(3) Department of Molecular Pathobiology, Mie University School of Medicine, Mie, Japan, JP |
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Abstract: | Peripheral blood lymphocytes obtained from children with acute lymphoblastic leukemia (ALL) at onset were studied for the expression of interleukin-2 (IL-2) receptor α-chain (CD25) by two-color flow-cytometric analysis. Stimulated with anti-CD3 monoclonal antibody (mAb) alone, CD25 expression was significantly suppressed in CD4+ T cells from 27 of 48 (56.3%) cases and in CD8+ T cells from 29 of 48 (60.4%) cases. When stimulated with anti-CD3 mAb plus phorbol 12-myristate 13-acetate (PMA), CD25 expression was clearly restored in certain cases of ALL. When PMA plus ionomycin were used for stimulation of T cells, CD25 was inducible in a majority of cases. Interestingly CD25 expression upon anti-CD3 mAb stimulation was recovered after complete remission had been achieved. These observations suggest the presence in ALL children at onset of an in vitro defect in the signal transduction pathway of the T-cell-receptor/CD3 complex, resulting in inefficient CD25 expression. However, immune-staining analysis indicated that protein kinase C was normally translocated from the cytosol fraction to the cell membrane fraction. The mobilization of cytoplasmic free calcium is also normal. Received: 27 March 1996 / Accepted: 23 December 1996 |
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Keywords: | Interleukin-2 receptor Protein kinase C Acute lymphoblastic leukemia Immunosuppression |
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