Induced and natural regulatory T cells in the development of inflammatory bowel disease. Inflamm Bowel Dis 2013 Jul;19(8):1772-88
Date
05/10/2013Pubmed ID
23656897Pubmed Central ID
PMC3690174DOI
10.1097/MIB.0b013e318281f5a3Scopus ID
2-s2.0-84883772859 (requires institutional sign-in at Scopus site) 146 CitationsAbstract
The mucosal immune system mediates contact between the host and the trillions of microbes that symbiotically colonize the gastrointestinal tract. Failure to tolerate the antigens within this "extended self" can result in inflammatory bowel disease (IBD). Within the adaptive immune system, the most significant cells modulating this interaction are Foxp3 regulatory T (Treg) cells. Treg cells can be divided into 2 primary subsets: "natural" Treg cells and "adaptive" or "induced" Treg. Recent research suggests that these subsets serve to play both independent and synergistic roles in mucosal tolerance. Studies from both mouse models and human patients suggest that defects in Treg cells can play distinct causative roles in IBD. Numerous genetic, microbial, nutritional, and environmental factors that associate with IBD may also affect Treg cells. In this review, we summarize the development and function of Treg cells and how their regulatory mechanisms may fail, leading to a loss of mucosal tolerance. We discuss both animal models and studies of patients with IBD suggesting Treg cell involvement in IBD and consider how Treg cells may be used in future therapies.
Author List
Mayne CG, Williams CBAuthor
Calvin B. Williams MD, PhD Chief, Professor in the Pediatrics department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsDisease Models, Animal
Forkhead Transcription Factors
Humans
Immune Tolerance
Inflammatory Bowel Diseases
Mice
T-Lymphocytes, Regulatory
