Abstract
Inflammatory bowel disease (IBD) is characterized by unrestrained T-cell activation that results in the production of a variety of inflammatory cytokines and other mediators. Understanding the mechanisms of T-cell regulation is therefore of significant importance to IBD and other forms of dysregulated-mucosal inflammation. An area that is of significant interest are the cell autonomous mechanisms of T-cell regulation through proteins that have natural inhibitory functions when expressed on T lymphocytes. One such molecule is carcinoembryonic antigen cell adhesion molecule 1 (CEACAM1). CEACAM1 is primarily an activation-induced cell-surface molecule that functions as a co-inhibitory receptor. Homophilic ligation of CEACAM1 on T cells leads to a signaling mechanism, which results in inhibition of a broad range T-cell functions. CEACAM1 therefore represents a new potential therapeutic target in the treatment of IBD.