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The ARNT-STAT3 axis regulates the differentiation of intestinal intraepithelial TCRαβ⁺CD8αα⁺ cells.

Abstract：

:Intestinal intraepithelial T cells contribute to the regulation of inflammatory responses in the intestine; however, the molecular basis for their development and maintenance is unknown. The aryl hydrocarbon receptor complexes with the aryl hydrocarbon receptor nuclear translocator (ARNT) and senses environmental factors, including gut microbiota. Here, we identify ARNT as a critical regulator of the differentiation of TCRαβ(+)CD8αα(+) intestinal intraepithelial T cells. Mice deficient in either ARNT or aryl hydrocarbon receptor show a greater than- eight-fold reduction in the number of TCRαβ(+)CD8αα(+) intestinal intraepithelial T cells. The number of TCRαβ(+)CD8αα(+) intestinal intraepithelial T cells is increased by treatment with an aryl hydrocarbon receptor agonist in germ-free mice and is decreased by antibiotic treatment. The Arnt-deficient precursors of TCRαβ(+)CD8αα(+) intestinal intraepithelial T cells express low amounts of STAT3 and fail to differentiate towards the TCRαβ(+)CD8αα(+) cell fate after IL-15 stimulation, a deficiency that is overcome by overexpression of Stat3. These data demonstrate that the ARNT-STAT3 axis is a critical regulator of TCRαβ(+)CD8αα(+) intestinal intraepithelial T-cell development and differentiation.

journal_name

Nat Commun

journal_title

Nature communications

authors

Nakajima K,Maekawa Y,Kataoka K,Ishifune C,Nishida J,Arimochi H,Kitamura A,Yoshimoto T,Tomita S,Nagahiro S,Yasutomo K

doi

10.1038/ncomms3112

subject

Has Abstract

pub_date

2013-01-01 00:00:00

pages

2112

issn

2041-1723

pii

ncomms3112

journal_volume

4

pub_type

杂志文章

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