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Author Yuan, Aping ♦ Yang, Hang ♦ Qi, Haili ♦ Cui, Jing ♦ Hua, Wei ♦ Li, Can ♦ Pang, Zhigang ♦ Zheng, Wei ♦ Cui, Guanglin
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ ANIMAL TISSUES ♦ ANTIBODIES ♦ BIOPSY ♦ DEXTRAN ♦ INFLAMMATION ♦ INJECTION ♦ LYMPHOCYTES ♦ LYMPHOKINES ♦ MICE ♦ PATHOGENESIS ♦ SODIUM ♦ SULFATES
Abstract Diverse T help (Th) cells play a crucial role in the processing and maintaining of chronic inflammation as seen in ulcerative colitis (UC). Th9, a novel subset of Th cells that primarily produces interleukin (IL)-9, has recently been associated with the development of inflammatory diseases. In this study, we evaluated the presentation of Th9 cells in inflamed tissues of human and experimental mouse UC, and examined the therapeutic efficiency of anti Th9 cytokine IL-9 in the experimental mouse UC. Using immunohistochemistry (IHC), we evaluated the presentation of Th9 cells labelled by transcriptional factor PU.1 in both human and dextran sulfate sodium (DSS) induced mouse colitis biopsies. The results showed that increased PU.1 positive Th9 cells were mainly located in the lamina propria in relative with the controls, intraepithelial Th9 cells can also be observed but at low density. Double IHCs revealed that most of PU.1 positive cells were CD3 positive lymphocytes in human UC specimens. Anti-IL-9 antibody injection for 2 weeks reduced the severity of inflammation in DSS induced colitis mice. Our results suggest that The Th9/IL-9 is involved in the pathogenesis of UC. - Highlights: • The density of novel PU.1 positive Th9 cells is significantly increased in both human and mouse colitis tissues. • PU.1 positive Th9 cells are predominately located in the inflamed lamina propria in both human and mouse colitis tissues. • Blocking of Th9 cytokine IL-9 by antibody injection suppresses the severity of inflammation in the bowel in colitis mice. • Novel Th9 cells contribute to the pathogenesis of UC.
ISSN 0006291X
Educational Use Research
Learning Resource Type Article
Publisher Date 2015-12-25
Publisher Place United States
Journal Biochemical and Biophysical Research Communications
Volume Number 468
Issue Number 4


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