T Cell-Specific Knockout of STAT3 Ameliorates Dextran Sulfate Sodium-Induced Colitis by Reducing the Inflammatory Response.
- Author:
Sun Ho KWON
1
;
Eun Bi SEO
;
Song Hee LEE
;
Chung Hyun CHO
;
Sung Joon KIM
;
Sang Jeong KIM
;
Hang Rae KIM
;
Sang Kyu YE
Author Information
- Publication Type:Original Article
- Keywords: T lymphocytes; STAT3 transcription factor; DSS-induced colitis; Cytokines; Homeostasis
- MeSH: Animals; Colitis*; Colitis, Ulcerative; Colon; Cytokines; Dextran Sulfate*; Dextrans*; Epithelial Cells; Homeostasis; Humans; Inflammation; Inflammatory Bowel Diseases; Interferons; Interleukin-10; Interleukin-17; Interleukin-6; Lymph Nodes; Mice; Peroxidase; Spleen; STAT3 Transcription Factor; T-Lymphocytes
- From:Immune Network 2018;18(4):e30-
- CountryRepublic of Korea
- Language:English
- Abstract: 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.
