Figure 7
Figure 7. Differential effect of soluble and coated Ab directed against α and β integrin chains on U1 cell adhesion and HIV-1 expression. Microtiter wells were coated with different Ab (1 μg/well) before seeding and stimulation of U1 cells (2 × 105 cells/mL). In parallel, U1 cells were resuspended at 2 × 105 cells/mL in medium enriched with the indicated Ab (10 μg/mL) before seeding and stimulation with PMA in the presence or absence of uPA. The same concentration of Ab was supplemented after 24 hours of cell culture. Cell adhesion (top panel) and virus expression (bottom panel) were measured 48 hours after cell seeding. The results shown were derived from 1 experiment representative of 3 independently performed experiments. Significantly enhanced cell adhesion was observed in all PMA-stimulated cells versus unstimulated cells (Nil; *P < .001). Furthermore, uPA increased PMA-stimulated cell adhesion (**P < .001 vs PMA alone). Significantly increased levels of cell adhesion were also observed when otherwise unstimulated U1 cells were incubated in wells coated with anti-CD29 mAb (°P < .001 vs Nil). Virus expression was significantly inhibited by uPA in all conditions (⋀P < .001 vs PMA), but not in uPA-treated, PMA-stimulated cells incubated with either soluble anti-CD29 or soluble anti-CD18 Ab- versus BSA-treated cells (*P < .001). Finally, significantly lower levels of HIV production were observed in PMA-stimulated U1 cells incubated in wells coated with anti-CD11b mAb (***P = .004).

Differential effect of soluble and coated Ab directed against α and β integrin chains on U1 cell adhesion and HIV-1 expression. Microtiter wells were coated with different Ab (1 μg/well) before seeding and stimulation of U1 cells (2 × 105 cells/mL). In parallel, U1 cells were resuspended at 2 × 105 cells/mL in medium enriched with the indicated Ab (10 μg/mL) before seeding and stimulation with PMA in the presence or absence of uPA. The same concentration of Ab was supplemented after 24 hours of cell culture. Cell adhesion (top panel) and virus expression (bottom panel) were measured 48 hours after cell seeding. The results shown were derived from 1 experiment representative of 3 independently performed experiments. Significantly enhanced cell adhesion was observed in all PMA-stimulated cells versus unstimulated cells (Nil; *P < .001). Furthermore, uPA increased PMA-stimulated cell adhesion (**P < .001 vs PMA alone). Significantly increased levels of cell adhesion were also observed when otherwise unstimulated U1 cells were incubated in wells coated with anti-CD29 mAb (°P < .001 vs Nil). Virus expression was significantly inhibited by uPA in all conditions (⋀P < .001 vs PMA), but not in uPA-treated, PMA-stimulated cells incubated with either soluble anti-CD29 or soluble anti-CD18 Ab- versus BSA-treated cells (*P < .001). Finally, significantly lower levels of HIV production were observed in PMA-stimulated U1 cells incubated in wells coated with anti-CD11b mAb (***P = .004).

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