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Prepublished online as a Blood First Edition Paper on May 1, 2003; DOI 10.1182/blood-2002-10-3293.
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Blood, 15 September 2003, Vol. 102, No. 6, pp. 1951-1958
CHEMOKINES
Involvement of CXCR4 and IL-2 in the homing and retention of human NK and NK T cells to the bone marrow and spleen of NOD/SCID mice
Katia Beider,
Arnon Nagler,
Ori Wald,
Suzanna Franitza,
Michal Dagan-Berger,
Hanna Wald,
Hilla Giladi,
Stefan Brocke,
Jacob Hanna,
Ofer Mandelboim,
Merav Darash-Yahana,
Eithan Galun, and
Amnon Peled
From the Gene Therapy Institute, Hadassah University Hospital, Jerusalem, Israel; the Department of Bone Marrow Transplantation, Chaim Sheba Medical Center, Tel Hashomer, Israel; the Department of Pathology, Hebrew University Hadassah Medical School, Jerusalem, Israel; and the Lautenberg Center for General and Tumor Immunology Oncology, Hadassah Medical School, Jerusalem, Israel.
Human natural killer (NK) and NK T cells play an important role in allogeneic bone marrow (BM) transplantation and graft-versus-leukemia (GVL) effect. The mechanisms by which these cells home to the BM and spleen are not well understood. Here we show that treatment of these cells with pertussis toxin and neutralizing antibodies to the chemokine receptor CXCR4 inhibited homing of the cells to the BM, but not the spleen, of NOD/SCID mice. The retention of NK and NK T cells within the spleen and BM was dependent on G i signaling and CXCR4 function. The chemokine receptors CXCR4 and CXCR3 are expressed predominantly on the cell surface of NK T cells. Following activation with interleukin-2 (IL-2), the levels of CXCR4 on NK and NK T cells decreased significantly. Treatment of cells with IL-2 inhibited their migration in response to CXCL12 and their homing and retention in the BM and spleen of NOD/SCID mice. In contrast to CXCR4, the expression levels of the chemokine receptor CXCR3 and the migration of cells in response to CXCL9 and CXCL10 increased after IL-2 treatment. Thus, down-regulation of CXCR4 and up-regulation of CXCR3 may direct the trafficking of cells to the site of inflammation, rather than to hematopoietic organs, and therefore may limit their alloreactive potential.
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