Regulated immune responses are essential to maintain intestinal homeostasis and require direct or indirect communication among cells. Communication that occurs among cells in the absence of direct contact is often through the use of cytokines and chemokines. Ulcerative colitis (UC) and Crohn's disease (CD) are chronic intestinal inflammatory bowel diseases (IBD). IBD is characterized by increased influx of immune cells to the mucosa of genetically susceptible hosts. The characteristic increase of inflammatory infiltrate is mainly of T cells recruited to the lamina propria (LP) by a multistep process that involves the integrated interactions and effects of adhesion molecules and chemokines (1). Numerous studies in IBD patients and in animal models of colitis have demonstrated that both inflammatory chemokines and their receptors are up-regulated in settings of active inflammation (2). More importantly, blockade or absence of various chemokine receptors attenuates disease in murine models of IBD. Thus, identifying chemokines and their receptors that are involved in intestinal inflammation provide promising targets for new drug development in the treatment of IBD.