Autoregulation of NFATc1/A expression facilitates effector T cells to escape from rapid apoptosis

被引：170

作者：

Chuvpilo, S

Jankevics, E

Tyrsin, D

Akimzhanov, A

Moroz, D

Jha, MK

Luehrmann, JS

Santner-Nanan, B

Feoktistova, E

König, T

Avots, A

Schmitt, E

Berberich-Siebelt, F

Schimpl, A

Serfling, E ^{[1
]}

机构：

[1] Univ Wurzburg, Inst Pathol, Dept Mol Pathol, D-97080 Wurzburg, Germany

[2] Univ Wurzburg, Inst Virol & Immunobiol, D-97080 Wurzburg, Germany

[3] Johannes Gutenberg Univ Mainz, Inst Immunol, D-55101 Mainz, Germany

[4] Latvian State Univ, Biomed Res & Study Ctr, LV-1067 Riga, Latvia

来源：

IMMUNITY | 2002年 / 16卷 / 06期

关键词：

D O I：

10.1016/S1074-7613(02)00329-1

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Threshold levels of individual NFAT factors appear to be critical for apoptosis induction in effector T cells. In these cells, the short isoform A of NFATc1 is induced to high levels due to the autoregulation of the NFATc1 promoter P1 by NFATs. P1 is located within a CpG island in front of exon 1, represents a DNase I hypersensitive chromatin site, and harbors several sites for binding of inducible transcription factors, including a tandemly arranged NFAT site. A second promoter, P2, before exon 2, is not controlled by NFATs and directs synthesis of the longer NFATc1/B+C isoforms. Contrary to other NFATs, NFATc1/A is unable to promote apoptosis, suggesting that NFATc1/A enhances effector functions without promoting apoptosis of effector T cells.

引用

页码：881 / 895

页数：15

共 60 条

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