NDLI: Ecto-nucleoside triphosphate diphosphohydrolase 7 controls Th17 cell responses through regulation of luminal ATP in the small intestine.

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Ecto-nucleoside triphosphate diphosphohydrolase 7 controls Th17 cell responses through regulation of luminal ATP in the small intestine.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ueda, Yoshiyasu Atarashi, Koji Okumura, Ryu Murakami, Masaaki Arima, Yasunobu Nishimura, Jun-ichi Kurakawa, Takashi Yamamoto, Masahiro Kiyono, Hiroshi Jeon, Seong Gyu Kinoshita, Makoto Maeda, Yuichi Ikeda, Kayo Okumura, Meinoshin Goto, Yoshiyuki Saiga, Hiroyuki Takeda, Kiyoshi Kunisawa, Jun Kusu, Takashi Honda, Kenya Kayama, Hisako
Description	Country affiliation: Japan Author Affiliation: Kusu T ( Laboratory of Immune Regulation, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.)
Abstract	Extracellular ATP is released from live cells in controlled conditions, as well as dying cells in inflammatory conditions, and, thereby, regulates T cell responses, including Th17 cell induction. The level of extracellular ATP is closely regulated by ATP hydrolyzing enzymes, such as ecto-nucleoside triphosphate diphosphohydrolases (ENTPDases). ENTPDase1/CD39, which is expressed in immune cells, was shown to regulate immune responses by downregulating the ATP level. In this study, we analyzed the immunomodulatory function of ENTPDase7, which is preferentially expressed in epithelial cells in the small intestine. The targeted deletion of Entpd7 encoding ENTPDase7 in mice resulted in increased ATP levels in the small intestinal lumen. The number of Th17 cells was selectively increased in the small intestinal lamina propria in Entpd7(-/-) mice. Th17 cells were decreased by oral administration of antibiotics or the ATP antagonist in Entpd7(-/-) mice, indicating that commensal microbiota-dependent ATP release mediates the enhanced Th17 cell development in the small intestinal lamina propria of Entpd7(-/-) mice. In accordance with the increased number of small intestinal Th17 cells, Entpd7(-/-) mice were resistant to oral infection with Citrobacter rodentium. Entpd7(-/-) mice suffered from severe experimental autoimmune encephalomyelitis, which was associated with increased numbers of CD4(+) T cells producing both IL-17 and IFN-Î³. Taken together, these findings demonstrate that ENTPDase7 controls the luminal ATP level and, thereby, regulates Th17 cell development in the small intestine.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1103067
Journal	The Journal of Immunology
Issue Number	2
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-01-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adenosine Triphosphate Metabolism Intestine, Small Immunology Pyrophosphatases Th17 Cells Animals Citrobacter Rodentium Encephalomyelitis, Autoimmune, Experimental Genetics Enterobacteriaceae Infections Gene Expression Regulation Intestinal Mucosa Microbiology Metagenome Mice Mice, Knockout Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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