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's disease (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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Authors | A Devito |
Journal | La Clinica terapeutica
(Clin Ter)
Vol. 166
Issue 2
Pg. e114-7
( 2015)
ISSN: 1972-6007 [Electronic] Italy |
PMID | 25945443
(Publication Type: Journal Article)
|
Chemical References |
- Biomarkers
- CXCL10 protein, human
- CXCR3 protein, human
- Chemokine CXCL10
- Receptors, CXCR3
- Interferon-gamma
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Topics |
- Animals
- Biomarkers
(blood)
- Chemokine CXCL10
(blood)
- Crohn Disease
(metabolism)
- Epithelial Cells
(metabolism)
- Humans
- Interferon-gamma
(physiology)
- Intestinal Mucosa
(metabolism)
- Mice
- Receptors, CXCR3
(metabolism)
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