Quantitative characterization and potential function of membrane Fas/APO-1 (CD95) receptors on leukaemic cells from chronic B and T lymphoid leukaemias

被引:32
作者
Kamihira, S
Yamada, Y
Hirakata, Y
Tsuruda, K
Sugahara, K
Tomonaga, M
Maeda, T
Tsukasaki, K
Atogami, S
Kobayashi, N
机构
[1] Nagasaki Univ, Sch Med, Dept Lab Med, Nagasaki 852, Japan
[2] Nagasaki Univ, Sch Med, Dept Haematol, Nagasaki 852, Japan
[3] Nagasaki Univ, Sch Pharmaceut Sci, Nagasaki 852, Japan
关键词
Fas/APO-1; apoptosis; ATL; flow cytometry; oncogenesis;
D O I
10.1046/j.1365-2141.1997.4963301.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The expression and function of the Fas-receptor (Fas-R) were examined in chronic lymphocytic leukaemia (CLL), hairy cell leukaemia-variant (HCL-v) and adult T-cell leukaemia (ATL). The expression of Fas-R in freshly isolated leukaemic cells was qualitatively and quantitatively different between each disease; faint in B-CLL, moderate in HCL-v and strong in ATL. Both full-length and alternatively spliced truncated forms of Fas mRNA were detected even in CLL B cells with faint to negative Fas-R, and Fas mRNA was also shown to be capable of increasing in vitro expression, i.e. the message was functional, Ln contrast, Fas-R expression on ATL cells was heterogenous and usually intense with a mean density approximately 3-fold higher than that of normal T cells, Fas-R was confirmed to have the potential function for anti-Fas monoclonal antibody-mediated cell death in vitro in Fas-R+ ATL cells, The expression level of Fas-R on the cells was higher in chronic than acute ATL (10360 v 6260 antibody-binding capacity per cell, mFas(ABC); P<0.05) and was inversely correlated with serum LDH activity, suggesting that the strong Fas-R accounts for the slow progression of chronic ATL and the negative Fas-R protects from Fas-mediated cell death. These results show that Fas-R expression on leukaemic cells is valuable in their characterization and perhaps their function, and may contribute to the progression and immune evasion of malignant clones.
引用
收藏
页码:858 / 865
页数:8
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