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IL-33 Protects Mice against DSS-Induced Chronic Colitis by Increasing Both Regulatory B Cell and Regulatory T Cell Responses as Well as Decreasing Th17 Cell Response.
- Source :
-
Journal of Immunology Research . 11/13/2018, p1-12. 12p. 1 Color Photograph, 2 Charts, 6 Graphs. - Publication Year :
- 2018
-
Abstract
- <bold>Background: </bold>Previously, we have reported that IL-33 functioned as a protective modulator in dextran sulfate sodium- (DSS-) induced chronic colitis by suppressing Th17 cell response in colon lamina propria and IL-33 induced both regulatory B cells (Bregs) and regulatory T cells (Tregs) in mesenteric lymph nodes (MLNs) of mice with DSS-induced acute colitis. Moreover, we speculated that IL-33 would promote the Treg or Breg responses leading to the attenuation of DSS-induced chronic colitis. So, we investigated the role of IL-33 on Bregs and Tregs in the MLN of DSS-induced chronic colitis mice.<bold>Methods: </bold>IL-33 was administered by intraperitoneal injection to mice with DSS-induced chronic colitis. Clinical symptoms, colon length, and histological changes were determined. The production of cytokines was measured by ELISA. The T and B cell subsets were measured by flow cytometry. The expression of mRNA of transcription factors was measured by quantitative real-time PCR.<bold>Results: </bold>We show that IL-33 treatment increases both Breg and Treg responses in the MLN of mice with DSS-induced chronic colitis. Moreover, IL-33 treatment also decreases Th17 cell response in the MLN of mice with DSS-induced chronic colitis.<bold>Conclusion: </bold>Our data provide clear evidence that IL-33 plays a protective role in DSS-induced chronic colitis, which is closely related to increasing Breg and Treg responses in the MLN of mice as well as suppressing Th17 cell responses. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 23148861
- Database :
- Academic Search Index
- Journal :
- Journal of Immunology Research
- Publication Type :
- Academic Journal
- Accession number :
- 132988168
- Full Text :
- https://doi.org/10.1155/2018/1827901