Blood regulatory T cells in inflammatory bowel disease, a systematic review, and meta-analysis.

• The frequency of CD4+CD25+CD127− and CD4+CD25+FoxP3+ Tregs was significantly lower in IBD cases compared to healthy subjects. • The active IBD cases showed a significantly lower frequency of Treg cells, compared to the remission cases. • Treg cell proportion was significantly lower in UC cases in comparison to healthy subjects. Inflammatory bowel disease (IBD) is an autoimmune disease involving various parts of the gastrointestinal (GI) tract, which includes Crohn's disease (CD) and ulcerative colitis (UC). Due to the contradictory results regarding the percentage of peripheral blood (PB) regulatory T cells (Tregs) in IBD patients, this meta-analysis aimed to determine the Tregs frequency in IBD patients. We searched PubMed, Web of Science, SCOPUS, and Google Scholar databases for relevant observational articles that analyzed and reported the frequency of PB Tregs in IBD patients and healthy control groups. After choosing the related articles by two reviewers, the data regarding the definition of Tregs and their frequencies in different groups were recorded. In 22 studies, the results showed a nonsignificant difference in the frequency of PB Tregs between IBD cases and control subjects (SMD: −0.27, 95 % CI: −0.78, 0.23). However, the frequency of CD4+CD25+CD127− (SMD: −0.89, 95 % CI: −1.52, −0.26) and CD4+CD25+FoxP3+ (SMD: −1.32, 95 % CI: −2.37, −0.26) Tregs were significantly lower in IBD cases, compared to healthy subjects. Also, UC cases and active IBD cases showed a significantly lower frequency of Treg cells, compared to controls and remission IBD cases, respectively (SMD: −0.68, 95 % CI: −1.24, −0.11 and SMD: −0.60, 95 % CI: −0.93, −0.27). Our study highlighted a probable decrease of Tregs in IBD patients, especially the patients with active states of the disease. The decrease of Treg cells might cause an imbalance in the immune system and the over-activation of auto-immune responses against the digestive tract. [ABSTRACT FROM AUTHOR]