T Cell-Specific Knockout of STAT3 Ameliorates Dextran Sulfate Sodium-Induced Colitis by Reducing the Inflammatory Response
Immune Network
;
: e30-2018.
Article
in English
| WPRIM
| ID: wpr-716247
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Spleen
/
T-Lymphocytes
/
Inflammatory Bowel Diseases
/
Colitis, Ulcerative
/
Cytokines
/
Dextran Sulfate
/
Dextrans
/
Interferons
/
Interleukin-6
/
Interleukin-10
Limits:
Animals
/
Humans
Language:
English
Journal:
Immune Network
Year:
2018
Type:
Article
Similar
MEDLINE
...
LILACS
LIS