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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
[Imbalance of CD4(+) T cell subgroups in ulcerative colitis]
Kang Chao1, Bi-hui Zhong, Sheng-hong Zhang
1Department of Gastroenterology, Sun Yat-sen University, Guangzhou 510080, China.
Objective:
To investigate the relationship of the imbalance of CD4(+) T cell subgroups and the pathogenesis of ulcerative colitis (UC).
Methods:
Peripheral blood samples were collected from 24 UC patients and 17 healthy donors. Then the phenotype of CD4(+) T cells and the major transcription factor expression of each subset were analyzed by flow cytometry and real-time PCR (polymerase chain reaction) respectively. The serum concentrations of major cytokines of each subgroup were measured by cytometric bead array (CBA) and ELISA (enzyme-linked immunosorbent assay).
Results:
(1) The proportion of Treg cells in the UC group was lower than the control group (6.7% ± 1.7% vs 7.9% ± 1.4%, P = 0.016), especially in active stage (6.4% ± 1.7%, P = 0.005). As compared with the control group, the expression of FOXP3 mRNA was lower in the UC Group (P = 0.020). And so was the serum concentration of TGF-β1 [(21 ± 8) µg/L vs (28 ± 7) µg/L, P = 0.026]. (2) There were no significant differences in Th1-related transcription factors and cytokines between two groups. (3) Th2 cells were higher in the UC group (2.7% ± 1.1% vs 1.6% ± 0.4%, P = 0.002), especially in active stage (2.8% ± 1.0%, P = 0.001). The expression of GATA-3 mRNA was 4.4 folds higher than that of the controls (P = 0.045). (4) Th17 cells were higher in the UC group (3.4% ± 1.8% vs 1.8% ± 0.7%, P = 0.005). And the RORγt mRNA expression was 13 folds higher in UC group (P = 0.001); the serum concentrations of IL-6 and IL-17 were higher in the UC group (both P < 0.05). (5) The ratios of Treg/Th2 and Treg/Th17 were significantly lower in the UC group and associated with disease activity (both P < 0.05).
Conclusion:
The imbalances of Th2, Treg and Th17 subgroups may play pivotal roles in the pathogenesis of UC.
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