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2015 ; 5
(ä): 12113
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Zbtb16 (PLZF) is stably suppressed and not inducible in non-innate T cells via T
cell receptor-mediated signaling
#MMPMID26178856
Zhang S
; Laouar A
; Denzin LK
; Sant'Angelo DB
Sci Rep
2015[Jul]; 5
(ä): 12113
PMID26178856
show ga
The transcription factor PLZF (promyelocytic leukemia zinc finger; zbtb16) is
essential for nearly all of the unique characteristics of NKT cells including
their rapid and potent response to antigen. In the immune system, zbtb16
expression is only found in innate cells. Conventional T cells that ectopically
express PLZF spontaneously acquire an activated, effector phenotype. Activation
induced expression of lineage defining transcription factors such as T-bet,
FoxP3, ROR?t, GATA3 and others is essential for naïve T cell differentiation into
effector T cells. In this study, we used sensitive genetic-based approaches to
assess the induction of PLZF expression in non-innate T cells by T cell receptor
(TCR)-mediated activation. Surprisingly, we found that PLZF was stably repressed
in non-innate T cells and that TCR-mediated signaling was not sufficient to
induce PLZF in conventional T cells. The inactivated state of PLZF was stably
maintained in mature T cells, even under inflammatory conditions imposed by
bacterial infection. Collectively, our data show that, in contrast to multiple
recent reports, PLZF expression is highly specific to innate T cells and cannot
be induced in conventional T cells via TCR-mediated activation or inflammatory
challenge.