SATB1 is required for CD8 coreceptor reversal.
SATB1 is required for CD8 coreceptor reversal.
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DOI:
10.1016/j.molimm.2008.07.007
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发表时间:
2008-11
影响因子:
3.6
通讯作者:
Tucker PW
中科院分区:
文献类型:
--
作者:
Nie H;Yao X;Maika SD;Tucker PW
Intrathymic signals induce the differentiation of immature CD4+CD8+ double positive (DP) thymocytes into mature CD4+ or CD8+ single positive (SP) T cells. The transcriptional mechanism by which CD8 lineage is determined is not fully understood. The best evidence, which favors the kinetic signaling/co-receptor reversal model, indicates that signaled DP thymocytes terminate CD8 transcription prior to their subsequent re-initiation of CD8 transcription and ultimate differentiation into CD8SP T cells. We and others have shown that CD8 lineage commitment is severely perturbed in mice in which expression of the transcription factor SATB1 is either conventionally knocked out or T cell-specifically knocked down. Here, we demonstrate that, as with normal thymocytes, cultured SATB1-deficient DP thymocytes inactivate CD8 coreceptor transcription following receipt of signals (PMA plus ionomycin) that mimic TCR-mediated positive selection. However, this terminated CD8 transcription is not re-initiated by signals (IL-7) conducive to CD8 differentiation in SATB1-deficient DP. We show that SATB1 specifically binds to a cis-regulatory element within the CD8 enhancer (E8III) known to be required for coreceptor reversal. A requirement in CD8 coreceptor reversal identifies SATB1 as an essential trans-regulator of CD8 lineage fate, whose action may be mediated via recruitment to the E8III DP enhancer.
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影响因子:
7.8
作者:
de Belle, I;Cai, ST;Kohwi-Shigematsu, T
通讯作者:
Kohwi-Shigematsu, T
影响因子:
16
作者:
Harker, N;Naito, T;Kioussis, D
通讯作者:
Kioussis, D
影响因子:
64.5
作者:
DICKINSON, LA;JOH, T;KOHWISHIGEMATSU, T
通讯作者:
KOHWISHIGEMATSU, T
影响因子:
32.4
作者:
Chong, MMW;Cornish, AL;Kay, TWH
通讯作者:
Kay, TWH
DOI:
10.1084/jem.178.3.941
发表时间:
1993-09-01
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Landry DB;Engel JD;Sen R
通讯作者:
Sen R