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January 28, 2008BloodOpen Access

CCL3 and CXCL12 regulate trafficking of mouse bone marrow NK cell subsets

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Authors

GBGiovanni BernardiniSapienza University of RomeGSGiuseppe SciumèCentre National de la Recherche ScientifiqueDBDaniela BosisioBrescia University

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Implication

Preclinical study reveals chemokine regulation of natural killer cell trafficking in mouse bone marrow, indicating coordinated control of immune cell maturation and peripheral migration.

Key Points

  • To determine how specific chemokines and chemokine receptors control the retention, maturation, and egress of natural killer (NK) cell subsets in mouse bone marrow.
  • Assessed surface expression of CCR1, CXCR3, and CXCR4 alongside in vitro chemotactic responses to CCL3, CXCL10, and CXCL12 across precursor, immature, and mature NK cell subsets.
  • Administered the CXCR4 antagonist AMD-3100 or exogenous CCL3 to C57BL/6 mice to evaluate in vivo mobilization of NK cell subsets between the bone marrow, peripheral blood, and spleen.
  • Precursor and mature NK cells expressed CCR1, CXCR3, and CXCR4, whereas immature NK cells expressed only CXCR4; mature bone marrow NK cells selectively migrated in response to CXCL12, CXCL10, and CCL3.
  • AMD-3100 administration induced marked depletion of immature and mature NK cells within the bone marrow, accompanied by an increase of these subsets in peripheral blood and spleen.
  • CCL3 administration selectively mobilized mature NK cells from the bone marrow, an effect linked to CCL3-mediated inhibition of CXCL12-dependent mature NK cell migration.

Cite This Study

Bernardini et al. (2008) studied this question.

synapsesocial.com/papers/6a6f2b5326770c2b8ddfde3ehttps://doi.org/10.1182/blood-2007-08-106203
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