蛋白激酶C激活可能参与成人T细胞白血病细胞CD3抗原的下调。

Possible involvement of protein kinase C activation in down-regulation of CD3 antigen on adult T cell leukaemia cells.

作者信息

Matsuda M, Maeda Y, Shirakawa C, Morita S, Koyama A, Horiuchi F, Hamazaki H, Irimajiri K, Horiuchi A

机构信息

Third Department of Internal Medicine, Kinki University School of Medicine, Osaka, Japan.

出版信息

Br J Haematol. 1994 Feb;86(2):399-401. doi: 10.1111/j.1365-2141.1994.tb04751.x.

DOI:10.1111/j.1365-2141.1994.tb04751.x

PMID:8199035

Abstract

The role of protein kinase C (PKC) system on CD3 expression on adult T-cell leukaemia (ATL) was examined. The down-regulation of CD3 on ATL cells is reportedly induced by CD3 down-regulating factor (CD3DF) contained in serum and culture supernatants of leukaemia cells from acute type ATL patients. After we cultured normal PBMC with a PKC inhibitor, H-7, CD3DF activity for PBMC was reduced significantly. Culture with H-7 of HTLV-1 transformed T cells, ATL-2 cells whose CD3 expression had been decreased, led to enhancement of CD3 expression in a time-dependent manner. These findings suggest that CD3DF may play an important role as a PKC system activator, resulting in CD3 down-regulation.

摘要

研究了蛋白激酶C（PKC）系统在成人T细胞白血病（ATL）中CD3表达上的作用。据报道，急性型ATL患者白血病细胞的血清和培养上清液中所含的CD3下调因子（CD3DF）可诱导ATL细胞上CD3的下调。在用PKC抑制剂H-7培养正常外周血单核细胞（PBMC）后，PBMC的CD3DF活性显著降低。用H-7培养HTLV-1转化的T细胞、CD3表达已降低的ATL-2细胞，导致CD3表达呈时间依赖性增强。这些发现表明，CD3DF可能作为PKC系统激活剂发挥重要作用，从而导致CD3下调。