Alterations of T Lymphocytes in Inflammatory Bowel Diseases

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Conclusion

Data from multiple experimental models to date provide strong support for the immunologic hypothesis that a dysregulated mucosal CD4+ T cell response to antigens of the enteric bacteria in a genetically susceptible host results in chronic intestinal inflammation. The host interaction with the flora is complex, but there are a select number of cells and molecules that are critical to this effort. When these key pathways are impaired, the host response to the bacterial flora results in IBD. The key effector cell responsible for disease in most instances is the CD4+ T cell. Although there is data in some systems that Th1 and Th2 subsets can reciprocally regulate one another, each of these CD4 T cell effector CD4 T cell subsets has been found to mediate colitis in various mouse models. There is no data at present that demonstrates that Th2 cells regulate Th1 cells in the intestine or vice versa, and thus experimental colitis is not explained as an imbalance between Th1 and Th2 subsets. At present the data are compatible with the concept that excessive responses of either the Th1 or Th2 effector subsets are detrimental and can result in inflammatory bowel disease, and that this is prevented in the normal host by the presence and function of regulatory cells, particularly CD4+ Tregs. It is unclear how many distinct subsets of regulatory cells are present in the intestine, or the role that each may play in regulating the mucosal immune response to commensal bacterial antigens.