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Expression of CD4 + forkhead box P3 (FOXP3) + regulatory T cells in inflammatory bowel disease
Author(s) -
WANG Yi,
LIU Xue Ping,
ZHAO Zhi Bin,
CHEN Jun Hao,
YU Cheng Gong
Publication year - 2011
Publication title -
journal of digestive diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 51
eISSN - 1751-2980
pISSN - 1751-2972
DOI - 10.1111/j.1751-2980.2011.00505.x
Subject(s) - inflammatory bowel disease , foxp3 , medicine , disease , cancer research , immunology , immune system
OBJECTIVE: Forkhead box P3 (FOXP3) plays an important role in the development and function of CD4 + regulatory T (Treg) cells. In this study the percentage of CD4 + FOXP3 + Treg cells in peripheral blood mononuclear cells (PBMC) and the frequency of Treg cells in the colonic mucosa of patients with inflammatory bowel disease (IBD) were investigated. METHODS: The percentage of CD4 + FOXP3 + Treg cells in PBMC was analyzed by flow cytometry. Immunohistochemistry was used to examine the FOXP3 + cells in the inflamed mucosa. Real‐time polymerase chain reaction and Western blot were used to detect the expressions of FOXP3 mRNA and protein in PBMC and mucosal biopsy specimens of IBD patients, respectively. RESULTS: Together with the decrease of percentage of Treg cells in PBMC, we found that the frequency of Treg cells increased significantly in inflamed mucosa of active or inactive Crohn's disease (CD) and ulcerative colitis (UC). The expressions of FOXP3 mRNA and protein increased in inflamed mucosa when compared with those in healthy controls, especially the FOXP3 mRNA in patients with active CD or UC. Interestingly, the expression of FOXP3 protein in active UC was higher than that in active CD. CONCLUSIONS: There was a decrease of CD4 + FOXP3 + Treg cells in peripheral blood and an accumulation of Treg cells in inflamed mucosa. These data suggested that the suppressive function of Treg cells may be partially inhibited and this could be an important factor in the recurrence of disease, especially in UC.