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Down-regulation of Fas-associated phosphatase-1 (FAP-1) in interleukin-2-activated T cells.

作者信息

Zhou Y W, Komada Y, Inaba H, Azuma E, Sakurai M

机构信息

Department of Pediatrics, Mie University School of Medicine, Japan.

出版信息

Cell Immunol. 1998 Jun 15;186(2):103-10. doi: 10.1006/cimm.1998.1297.

DOI:10.1006/cimm.1998.1297
PMID:9665752
Abstract

Peripheral T cells are resistant to Fas receptor (FasR/CD95)-mediated apoptosis. After prolonged treatment with interleukin-2 (IL-2), these T cells develop a Fas-sensitive phenotype. To clarify the molecular mechanism of apoptosis susceptibility, mRNA expression of FasR-associated proteins [Fas-associating protein with death domain (FADD), receptor-interacting protein (RIP), and Fas-associated phosphatase-1 (FAP-1)] has been investigated in IL-2 activated T cells. Competitive reverse transcriptase-polymerase chain reaction analysis revealed that FADD and RIP mRNA were equally expressed in freshly isolated resting T cells and IL-2-activated T cells. In contrast, FAP-1 mRNA was produced more abundantly by Fas-resistant resting T cells than by Fas-sensitive activated T cells. These findings suggested that sensitivity to FasR-mediated apoptosis in T cells could be correlated with down-regulation of FAP-1 expression. Additionally, CD45RO+ memory T cells expressed a larger amount of FAP-1 mRNA than did CD45RA+ naive T cells.

摘要

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