Figure 5.
Figure 5. Enrichment of the CD16– subset in the migrated peripheral NK cells to CXCL12-α. The presence of the various NK populations in the migrated NK cells presented in Figure 4 was analyzed by quadruple staining. The percentage of increase or decrease of the CD16– or CD16+ subsets was calculated with regard to the starting point when no chemokine was present (100%). Migration was performed to CXCL9 (A), CXCL10 (B), and CXCL12-α (C). (D-G) Contour histogram of the CD16 phenotype of the migrated NK cells to CXCL9 (E), CXCL10 (F), and CXCL12-α (G). Control (D) represents the spontaneous migration when no chemokine was added. The percentages of CD16– and CD16+ subsets in the NK cells that spontaneously migrated when no chemokine was present were similar to those observed in the peripheral blood. Figure shows 1 representative experiment of 3 performed.

Enrichment of the CD16 subset in the migrated peripheral NK cells to CXCL12-α. The presence of the various NK populations in the migrated NK cells presented in Figure 4 was analyzed by quadruple staining. The percentage of increase or decrease of the CD16 or CD16+ subsets was calculated with regard to the starting point when no chemokine was present (100%). Migration was performed to CXCL9 (A), CXCL10 (B), and CXCL12-α (C). (D-G) Contour histogram of the CD16 phenotype of the migrated NK cells to CXCL9 (E), CXCL10 (F), and CXCL12-α (G). Control (D) represents the spontaneous migration when no chemokine was added. The percentages of CD16 and CD16+ subsets in the NK cells that spontaneously migrated when no chemokine was present were similar to those observed in the peripheral blood. Figure shows 1 representative experiment of 3 performed.

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