Immune Netw.
2018 Aug;18(4):e30. 10.4110/in.2018.18.e30.
T Cell-Specific Knockout of STAT3 Ameliorates Dextran Sulfate Sodium-Induced Colitis by Reducing the Inflammatory Response
- Affiliations
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- 1Department of Pharmacology and Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea. sangkyu@snu.ac.kr
- 2Neuro-Immune Information Storage Network Research Center, Seoul National University College of Medicine, Seoul 03080, Korea.
- 3Biomedical Science Project (BK21[PLUS]), Seoul National University College of Medicine, Seoul 03080, Korea.
- 4Department of Physiology and Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
- 5Department of Anatomy and Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
- 6Ischemia/Hypoxic Disease Institute, Seoul National University College of Medicine, Seoul 03080, Korea.
- KMID: 2419775
- DOI: http://doi.org/10.4110/in.2018.18.e30
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.
MeSH Terms
-
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
Cytokines
Dextran Sulfate
Dextrans
Interferons
Interleukin-10
Interleukin-17
Interleukin-6
Peroxidase
STAT3 Transcription Factor
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