Figure 7
CXCR4 and S1P5 responsiveness are modulated on mature NK cells. (A-B) BM cells were isolated from WT and S1P5−/− (A) or Cxcr4+/1013 (B) mice and migration of CD27low NK cells toward S1P or CXCL12 gradients was measured. (C) Spleen cells from WT mice were incubated for 2 hours in serum-free medium supplemented or not with S1P (10−8M) or CXCL12 (50 ng/mL). Migration of CD27low NK cells toward S1P or CXCL12 gradients was then assessed. (D-F) Lymphocytes were isolated from blood, spleen, and BM. Migration of mature NK cells toward S1P (D), CXCL12 (E), and CCL5 (F) gradients was assayed. The migration index is calculated as the ratio between the number of cells migrating in the chemokine and in the control (without chemokine) condition. Data are the mean ± SD of 4-5 independent experiments with duplicates.

CXCR4 and S1P5 responsiveness are modulated on mature NK cells. (A-B) BM cells were isolated from WT and S1P5−/− (A) or Cxcr4+/1013 (B) mice and migration of CD27low NK cells toward S1P or CXCL12 gradients was measured. (C) Spleen cells from WT mice were incubated for 2 hours in serum-free medium supplemented or not with S1P (10−8M) or CXCL12 (50 ng/mL). Migration of CD27low NK cells toward S1P or CXCL12 gradients was then assessed. (D-F) Lymphocytes were isolated from blood, spleen, and BM. Migration of mature NK cells toward S1P (D), CXCL12 (E), and CCL5 (F) gradients was assayed. The migration index is calculated as the ratio between the number of cells migrating in the chemokine and in the control (without chemokine) condition. Data are the mean ± SD of 4-5 independent experiments with duplicates.

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