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

Kohei Nakajima, Yoichi Maekawa, Keiko Kataoka, Chieko Ishifune, Jun Nishida, Hideki Arimochi, Akiko Kitamura, Takayuki Yoshimoto, Shuhei Tomita, Shinji Nagahiro and Koji Yasutomo ()
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Kohei Nakajima: Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto
Yoichi Maekawa: Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto
Keiko Kataoka: Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto
Chieko Ishifune: Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto
Jun Nishida: Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto
Hideki Arimochi: Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto
Akiko Kitamura: Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto
Takayuki Yoshimoto: Institute of Medical Science, Tokyo Medical University, 6-1-1 Shinjuku
Shuhei Tomita: Tottori University Faculty of Medicine, 86 Nishi-machi
Shinji Nagahiro: Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto
Koji Yasutomo: Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto

Nature Communications, 2013, vol. 4, issue 1, 1-11

Abstract: 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.

Date: 2013
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DOI: 10.1038/ncomms3112

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