Fig. 2.
Fig. 2. Comparison of secondary lymphoid-tissue chemokine (SLC)- and EBI1-ligand chemokine (ELC)-induced adhesion of adult T-cell leukemia (ATL) cells under static conditions. / (A) Comparison of SLC- and ELC-induced adhesion of ATL cells from patients with and without lymphoid organ involvement to human umbilical vein-derived endothelial cells (HUVECs) under static conditions. Cells (2 × 105/well), which had been labeled with 51Cr, were incubated with SLC or ELC at a concentration of 30 ng/ml at 37°C for 30 minutes and were added to the well containing IL-1β–activated HUVECs. The plates were incubated at 37°C for 30 minutes and then gently washed, and radioactivity of the adherent cells in each well was counted. The cells are as follows: control CD4+CD45RO+ T cells (A, closed squares) and ATL cells from patients without (B, patients 1 through 12) and with lymphoid organ involvement (C, patients 13 through 28). ATL cells from patients with lymphoid organ involvement were blocked with 100 ng/ml pertussis toxin (PTX) for 1.5 hours at 37°C (C+PT) or with anti-CD18 mAb, 7E4 (20 μg/ml) for 20 minutes at room temperature (C+CD18 Ab) before adding of chemokines. The data are expressed as the mean percentage of the binding of indicated cells from triplicate experiments. The statistical analysis was performed using Student t test. (B) Comparison of SLC- and ELC-induced adhesion of ATL cells from patients with and without lymphoid organ involvement to ICAM-1 under static conditions. The 96-well culture plates were coated with ICAM-1 protein (25 ng/well).

Comparison of secondary lymphoid-tissue chemokine (SLC)- and EBI1-ligand chemokine (ELC)-induced adhesion of adult T-cell leukemia (ATL) cells under static conditions.

(A) Comparison of SLC- and ELC-induced adhesion of ATL cells from patients with and without lymphoid organ involvement to human umbilical vein-derived endothelial cells (HUVECs) under static conditions. Cells (2 × 105/well), which had been labeled with 51Cr, were incubated with SLC or ELC at a concentration of 30 ng/ml at 37°C for 30 minutes and were added to the well containing IL-1β–activated HUVECs. The plates were incubated at 37°C for 30 minutes and then gently washed, and radioactivity of the adherent cells in each well was counted. The cells are as follows: control CD4+CD45RO+ T cells (A, closed squares) and ATL cells from patients without (B, patients 1 through 12) and with lymphoid organ involvement (C, patients 13 through 28). ATL cells from patients with lymphoid organ involvement were blocked with 100 ng/ml pertussis toxin (PTX) for 1.5 hours at 37°C (C+PT) or with anti-CD18 mAb, 7E4 (20 μg/ml) for 20 minutes at room temperature (C+CD18 Ab) before adding of chemokines. The data are expressed as the mean percentage of the binding of indicated cells from triplicate experiments. The statistical analysis was performed using Student t test. (B) Comparison of SLC- and ELC-induced adhesion of ATL cells from patients with and without lymphoid organ involvement to ICAM-1 under static conditions. The 96-well culture plates were coated with ICAM-1 protein (25 ng/well).

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