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

First Author  Nakajima K Year  2013
Journal  Nat Commun Volume  4
Pages  2112 PubMed ID  23836150
Mgi Jnum  J:205701 Mgi Id  MGI:5546272
Doi  10.1038/ncomms3112 Citation  Nakajima K, et al. (2013) The ARNT-STAT3 axis regulates the differentiation of intestinal intraepithelial TCRalphabeta(+)CD8alphaalpha(+) cells. Nat Commun 4:2112
abstractText  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 TCRalphabeta(+)CD8alphaalpha(+) intestinal intraepithelial T cells. Mice deficient in either ARNT or aryl hydrocarbon receptor show a greater than- eight-fold reduction in the number of TCRalphabeta(+)CD8alphaalpha(+) intestinal intraepithelial T cells. The number of TCRalphabeta(+)CD8alphaalpha(+) 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 TCRalphabeta(+)CD8alphaalpha(+) intestinal intraepithelial T cells express low amounts of STAT3 and fail to differentiate towards the TCRalphabeta(+)CD8alphaalpha(+) 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 TCRalphabeta(+)CD8alphaalpha(+) intestinal intraepithelial T-cell development and differentiation.
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