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Blood, 15 March 2005, Vol. 105, No. 6, pp. 2428-2435.
Prepublished online as a Blood First Edition Paper on November 9, 2004; DOI 10.1182/blood-2004-09-3458.
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Submitted September 8, 2004
Accepted November 3, 2004
NK cells that are activated by CXCL10 can kill tumor dormant cells that resist CTL-mediated lysis and can express B7-H1 that stimulates T cells
Aurore Saudemont, Nathalie Jouy, Dominique Hetuin, and Bruno Quesnel*
Institut de Recherche sur le Cancer de Lille, INSERM Unite 524, Lille, France; Institut Federatif de Recherche 114, Lille, France
Institut Federatif de Recherche 114, Lille, France
Institut de Recherche sur le Cancer de Lille, INSERM Unite 524, Lille, France; Institut Federatif de Recherche 114, Lille, France; Service des Maladies du Sang, Centre Hospitalier et Universitaire de Lille, Lille, France
* Corresponding author; email: brunoquesnel{at}hotmail.com.
Tumor dormancy is a phenomenon where small numbers of tumor cells persist in the host for months or years. We previously showed in the DA1-3b/C3H mouse model of acute myeloid leukemia that dormant tumor cells resist CTL-mediated killing because they over-express B7-H1. Here, we vaccinated mice with DA1-3b cells transduced with CXCL10. Vaccinated mice developed a strong systemic immunity that led to the cure of established leukemia without persistence of dormant tumor cells. In vivo depletion of NK cells from the mice abrogated the protective effect of the vaccine. Long-term persistent leukemic cells resist CTL-mediated lysis, but were killed by NK cells from DA1-3b/CXCL10 vaccinated mice. These NK cells expressed B7-H1. Recombinant CXCL10, CXCL9, CXCL11, and CXCL12 chemokines induced expression of B7-H1 on mouse and human NK cells in vitro. Mouse and human B7-H1+ NK cells induced proliferation of T cells and production of IFN- and TNF- in vitro, and in vivo blocking of B7-H1 inhibited the protective effect of vaccination. Thus, CXCL10 induces anti-leukemic immunity, at least partially by stimulating NK cells to express B7-H1+. This anti-tumor effect is in contrast to B7-H1's effect when expressed on tumour cells, as it stops cytotoxic lymphocytes from killing those tumour cells.
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