Nagaishi T, Chen Z, Chen L, Iijima H, Nakajima A, Blumberg R S
Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Mucosal Immunol. 2008 Nov;1 Suppl 1(0 1):S39-42. doi: 10.1038/mi.2008.50.
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.
炎症性肠病(IBD)的特征是T细胞不受控制地激活,导致产生多种炎性细胞因子和其他介质。因此,了解T细胞调节机制对于IBD和其他形式的失调性黏膜炎症具有重要意义。一个备受关注的领域是T细胞通过在T淋巴细胞上表达时具有天然抑制功能的蛋白质进行自我调节的机制。癌胚抗原细胞粘附分子1(CEACAM1)就是这样一种分子。CEACAM1主要是一种激活诱导的细胞表面分子,作为共抑制受体发挥作用。T细胞上CEACAM1的同源性连接导致一种信号传导机制,从而抑制广泛的T细胞功能。因此,CEACAM1代表了IBD治疗中的一个新的潜在治疗靶点。