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자료유형
학술저널
저자정보
Sun-Ho Kwon (Seoul National University College of Medicine) Eun-Bi Seo (Seoul National University College of Medicine) Song-Hee Lee (Seoul National University College of Medicine) Chung-Hyun Cho (Seoul National University College of Medicine) Sung Joon Kim (Seoul National University College of Medicine) Sang Jeong Kim (Seoul National University College of Medicine) Hang-Rae Kim (Seoul National University College of Medicine) Sang-Kyu Ye (Seoul National University College of Medicine)
저널정보
대한면역학회 Immune Network Immune Network Vol.18 No.4
발행연도
2018.8
수록면
41 - 54 (14page)

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Signal transducer and activator of transcription 3 (STAT3) has a crucial role in various autoimmune disorders including, inflammatory bowel disease (IBD). Our previous study demonstrated that STAT3 activation by IL-6 in colonic epithelial cells exacerbates experimental ulcerative colitis. Activated T lymphocytes are also found in ulcerative colitis patients with intestinal inflammation, but the role of STAT3 in T cells remains elusive. To determine the STAT3 function of T cells in intestinal inflammation, we generated T cell-specific STAT3 knockout (KO) mice and used dextran sulfate sodium (DSS) to induce colitis. In this study, we demonstrated that T cell-specific STAT3 deletion alleviated DSS-induced colitis in mice, resulting in reduced histological scores and myeloperoxidase (MPO) activity. Importantly, the population of T cells in the spleen and lymph nodes was significantly decreased in the control and DSS-induced groups of STAT3 KO mice. In addition, STAT3 deficiency in T cells markedly reduced the production of interferon (IFN)-γ, IL-6, and IL-17A, whereas IL-10 secretion was increased. Collectively, the results suggest that STAT3 in T cells may be a therapeutic target in ulcerative colitis by balancing the immune response through T cell homeostasis.

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ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2018-517-003392099