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Cardiovascular Research Advance Access first published online on February 5, 2008
This version [Corrected Proof] published online on March 15, 2008

Cardiovascular Research, doi:10.1093/cvr/cvn029
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Understanding the immunoangiostatic CXC chemokine network

Maria Luisa Balestrieri1,{dagger}, Antonio Balestrieri1,{dagger}, Francesco Paolo Mancini2 and Claudio Napoli3,*

1 Department of Biochemistry and Biophysics, 1st School of Medicine, II University of Naples, Naples 80138, Italy
2 Department of Biological and Environmental Sciences, University of Sannio, Benevento, Italy
3 Department of General Pathology, Division of Clinical Pathology and Excellence Research Center on Cardiovascular Diseases, 1st School of Medicine, II University of Naples, Via de Crecchio 7, Naples 80138, Italy

* Corresponding author. Tel: +39 081 5667567; fax: +39 081 450169. E-mail address: claunap{at}tin.it

Chemokines, originally discovered as mediators of directional migration of immune cells to sites of inflammation and injury, have a function beyond their role in leukocyte chemotaxis. Indeed, they participate in organ development, angiogenesis, tumourigenesis and, more importantly, in the immune response. The chemokine family characterized by four highly conserved cysteine amino acid residues, with two cysteine residues (C) and a non-cysteine amino acid (X) between them (CXC), is known for its ability to promote trafficking of various leukocytes and to regulate angiogenesis and vascular remodelling. Intriguingly, the presence or absence of a structural-functional domain constituted by glutamic acid–leucine–arginine motif that precedes the first cysteine amino acid residue accounts for their unique property to induce or inhibit angiogenesis (angiogenic or angiostatic activity). The ability of CXC chemokine receptor 3 to promote Th1-dependent immunity and, at the same time, inhibit angiogenesis (immunoangiostasis) is of critical importance for inducing tumour regression. Agents that are able to inhibit angiogenic activities or promote angiostatic activities of CXC chemokines are future targets for research on cancer treatment. Here, we review insights on CXC chemokines in the context of immunoangiostasis and vascular damage.

KEYWORDS Immunoangiostasis; Chemokines; CXCR3


Time for primary review: 20 days

{dagger} These authors contributed equally to this review.


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