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Blood, 1 April 2008, Vol. 111, No. 7, pp. 3626-3634.
Prepublished online as a Blood First Edition Paper on January 28, 2008; DOI 10.1182/blood-2007-08-106203.
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Submitted August 10, 2007
Accepted January 24, 2008
CCL3 and CXCL12 regulate trafficking of mouse bone marrow NK cell subsets
Giovanni Bernardini*, Giuseppe Sciume, Daniela Bosisio, Stefania Morrone, Silvano Sozzani, and Angela Santoni
Department of Experimental Medicine, Istituto Pasteur, Fondazione Cenci Bolognetti, University of Rome "La Sapienza", Rome, Italy
Department of Biomedical Sciences and Biotechnologies, University of Brescia, Brescia, Italy
* Corresponding author; email: giovanni.bernardini{at}uniroma1.it.
Herein we have analyzed chemokine involvement in the trafficking of developing and mature mouse NK cells in the bone marrow (BM). We observed drastic changes of CCR1, CXCR3 and CXCR4 expression and function during progression from NK cell precursors (pNK) to immature DX5- (iNK) and mature DX5+ (mNK) NK cells. pNK and mNK cells expressed the three receptors, while only CXCR4 was detected on iNK cells. Correspondingly, mNK cells migrated to CXCL12, CXCL10 and CCL3, and pNK and iNK cells to CXCL12, whereas pNK cells migrated to CCL3 and CXCL10 only after CXCL12 stimulation.
In regard to BM, peripheral blood and spleen mNK cell populations, our results show that CXCL12, CXCL10 and CCL3 preferentially affected BM mNK cell migration. Administration of the CXCR4 antagonist, AMD-3100, to C57BL/6 mice induced strong reduction of mNK and iNK cell in the BM and increased their number in blood and spleen. Conversely, CCL3 administration selectively mobilized mNK cells from the BM and this effect correlated with its ability to inhibit CXCL12-mediated mNK cell responses in vitro. Our results suggest that the combined action of chemokines selectively regulates localization of NK cell subsets in the BM and direct their maturation and migration to the periphery.
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