Abstract
Many studies have shown that chemokine (C-X-C motif) receptor (CXCR)3 and its ligand chemokines, as monokine induced by interferon (IFN)-γ (MIG), interferon-γ inducible protein (IP-10) and IFN-inducible T cell-α chemoattractant (I-TAC), are strongly overexpressed both in the intestinal mucosa of mice with experimental colitis, and in patients with Crohn'sdisease (CD) in lymphocytes, in macrophages and in epithelial cells. IFN-γ induces CXCR3 and its chemokines expression in epithelial intestinal cells; these chemokines are important for the recruitment of granulocytes and mononuclear cells, thus for the maintenance of inflammation in CD. Serum IP-10 levels might reflect CD disease activity, and it may be a marker for the responsiveness of patients to treatments. However other studies are needed to document the use of IP-10 in clinical setting. Attempts are currently underway to inhibit CXCR3 or its chemokines in CD as a possible therapy of CD.
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