Th17 cell differentiation proceeds independently of IRF8

被引：7

作者：

Newman, Dane M. ^{[1
,2
]}

Leung, Patrick S. K. ^{[1
,2
]}

Putoczki, Tracy L. ^{[1
,2
]}

Nutt, Stephen L. ^{[1
,2
]}

Cretney, Erika ^{[1
,2
]}

机构：

[1] Walter & Eliza Hall Inst Med Res, Parkville, Vic, Australia

[2] Univ Melbourne, Dept Med Biol, Parkville, Vic, Australia

来源：

IMMUNOLOGY AND CELL BIOLOGY | 2016年 / 94卷 / 08期

基金：

英国医学研究理事会;

关键词：

T-CELLS; TRANSCRIPTION FACTOR; REGULATORY NETWORK; LINEAGE; MICE; IMMUNODEFICIENCY; EXPRESSION;

D O I：

10.1038/icb.2016.33

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The transcriptional repressor/activator interferon regulatory factor 8 (IRF8) modulates the differentiation of a multitude of hematopoietic lineages. However, the role of IRF8 in CD4(+) T-cell development is less well defined, with a recent study implicating IRF8 as an intrinsic repressor of interleukin-17 (IL-17) expressing T helper type 17 (Th17) cell differentiation. Using an IRF8-EGFP reporter strain we have confirmed that IRF8 is expressed in all T helper lineages, including Th17 cells. The loss of IRF8 did not affect Th17 differentiation in vitro, beyond a small increase in IL-22 expression. Moreover, IRF8 deficiency did not enhance the Th17 immune response in experimental T-cell transfer colitis. Together, these results suggest that IRF8 does not play an essential intrinsic role in Th17 cell differentiation.

引用

页码：796 / 801

页数：6

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