| Autor: |
Gao, H., Lee, B.-N., Talpaz, M., Donato, N. J., Cortes, J. E., Kantarjian, H. M., Reuben, J. M. |
| Předmět: |
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| Zdroj: |
Leukemia (08876924); Nov2005, Vol. 19 Issue 11, p1905-1911, 7p, 1 Diagram, 5 Charts, 2 Graphs |
| Abstrakt: |
Although imatinib mesylate (IM) is highly effective at inducing complete cytogenetic remission in patients with chronic myelogenous leukemia (CML), it is known to suppress T-cell proliferation in vitro. As cytokines are required for T-cell proliferation, we investigated the effects of IM on cytokine synthesis by T cells of CML patients by assessing cytokine synthesis by activated CD4+ and CD8+ T cells in vitro. The activation of T cells in the whole blood of IM-treated patients (CML-IM) with Staphylococcus enterotoxin B resulted in significantly lower percentages of CD4+ T cells that synthesized interleukin 2 (P=0.017), interferon-gamma (P=0.010), and tumor necrosis factor-alpha (P=0.009) than did the activated T cells of control subjects. The addition of exogenous IM to the cultures of peripheral blood mononuclear cells of CML-IM patients reduced Th1 cytokine synthesis by the CD4+ T cells. Furthermore, IM therapy at clinical doses suppressed the tyrosine phosphorylation of ZAP70. These findings suggest that inhibition of ZAP70 signaling pathway and suppression of Th1 cytokine synthesis by CD4+ T cells required the presence of IM at the time of T-cell activation through the T-cell receptor.Leukemia (2005) 19, 1905–1911. doi:10.1038/sj.leu.2403933; published online 8 September 2005 [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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