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Blood, 1 February 2005, Vol. 105, No. 3, pp. 931-939.
Prepublished online as a Blood First Edition Paper on September 28, 2004; DOI 10.1182/blood-2004-03-0799.
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Submitted March 2, 2004
Accepted September 16, 2004
Chemokine receptor expression in EBV-associated lymphoproliferation in hu/SCID mice: implications for CXCL12/CXCR4 axis in lymphoma generation
Erich Piovan*, Valeria Tosello, Stefano Indraccolo, Anna Cabrelle, Ilenia Baesso, Livio Trentin, Rita Zamarchi, Hirokazu Tamamura, Nobutaka Fujii, Gianpietro Semenzato, Luigi-Chieco Bianchi, and Alberto Amadori
Department of Oncology and Surgical Sciences, Oncology Section, University of Padua, Padua, Italy
Department of Oncology and Surgical Sciences, Oncology Section, University of Padua, Padua, Italy; Istituto Nazionale per la Ricerca sul Cancro-IST, Genua, Italy; Azienda Ospedaliera Padova, Padua, Italy
Department of Clinical and Experimental Medicine, Clinical Immunology Branch, University of Padua, Padua, Italy; Venetian Institute for Molecular Medicine, Padua, Italy
Department of Oncology and Surgical Sciences, Oncology Section, University of Padua, Padua, Italy; Azienda Ospedaliera Padova, Padua, Italy
Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan
* Corresponding author; email: erich.piovan{at}unipd.it.
The mechanisms by which intraperitoneal injection of peripheral blood mononuclear cells (PBMC) from Epstein-Barr virus (EBV) seropositive donors into severe combined immunodeficient (SCID) mice gives rise to lymphomas (hu/SCID tumors) are far from clear. This study addressed whether chemokine receptors and their ligands could be implicated in this experimental model. CXCR4 was found to be highly expressed in hu/SCID tumors; surface expression of CXCR4 was prevalently limited to a tumor cell subset poorly expressing CD23, whereas the CXCR4 ligand, CXCL12, was predominantly expressed by the tumor subpopulation expressing CD23. In vitro inhibition of this autocrine/paracrine CXCL12/CXCR4 axis significantly inhibited lymphoma proliferation and survival. Furthermore, CXCL12 was expressed in cells recovered from the mouse peritoneal cavity early after PBMC transfer as well as by EBV-transformed B cells, but not by resting or activated B lymphocytes; also lymphoma development was associated with a dramatic increase in the levels of murine CXCL12 present in the peritoneal cavity. Finally, antagonizing the CXCL12/CXCR4 axis in vivo strongly counteracted lymphoma development. These studies demonstrate that CXCL12 expression may be associated with EBV infection and suggest that the CXCR4/CXCL12 axis may participate in EBV-associated lymphomagenesis process in immunodeficient hosts.
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