Abstract
Stress has long been postulated to influence the progression of inflammatory bowel disease (IBD) by mechanisms such as the interaction of neuroendocrine and immune system, abnormalities of epithelial ions secretion and passage of macromolecules into the lamina propria. There is some evidence of a dysregulation of the balance of proand antiinflammatory cytokines and T helper lymphocyte subsets in chronic intestinal inflammation. Studies in humans and in animal models indicate that stress skews the balance to response. CD26 is a cell surface ecto-enzyme with dipeptidyl peptidase IV (DPP IV; EC 3.4.14.5) activity expressed in different tissues, including a subset of human resting T cells. DPPIV is a serine protease with unique enzyme activity that can cleave off terminal dipeptides from polypeptides and proteins having either L-proline or L-arginine at the penultimate position. CD26 is involved in T cell migration through endothelial cell monolayers and also serves as membrane binding protein for ecto adenosine diaminase (ADA) . It has earlier been demonstrated that high expression of CD26 defines a type phenotype with enhanced production of like cytokines, namely
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