Figure 3.
Figure 3. Inhibition of cytoadhesion of FCR3 rIECSA to endothelial cells using anti–RSP-2 mAbs. 40μL suspension of 107 rIECSA/mL was incubated for 2 hours at 37°C on a confluent monolayer of Sc1D cells grown on 12 dot IFA slides in the presence of different concentrations of mAbs. Slides were washed and adherent rIEs counted. Results are expressed as mean ± SD percent inhibition of control. (A) Inhibition of rIECSA cytoadhesion in the presence of different concentrations of mAbs B4, C10, and D10. (B) Inhibition of rIECSA cytoadhesion of laboratory strains from different geographical areas, FCBR, BXII, SUK, HB, and IBR to Sc1D. (C) Placental isolates from Cameroonian women by anti–RSP-2 mAb B4. (D) Inhibition of rIECSA cytoadhesion to Sc1D by different concentrations of mAb B4 mixed together with 2 × 107 rIECSA under flow conditions at 0.05 Pa.

Inhibition of cytoadhesion of FCR3 rIECSA to endothelial cells using anti–RSP-2 mAbs. 40μL suspension of 107 rIECSA/mL was incubated for 2 hours at 37°C on a confluent monolayer of Sc1D cells grown on 12 dot IFA slides in the presence of different concentrations of mAbs. Slides were washed and adherent rIEs counted. Results are expressed as mean ± SD percent inhibition of control. (A) Inhibition of rIECSA cytoadhesion in the presence of different concentrations of mAbs B4, C10, and D10. (B) Inhibition of rIECSA cytoadhesion of laboratory strains from different geographical areas, FCBR, BXII, SUK, HB, and IBR to Sc1D. (C) Placental isolates from Cameroonian women by anti–RSP-2 mAb B4. (D) Inhibition of rIECSA cytoadhesion to Sc1D by different concentrations of mAb B4 mixed together with 2 × 107 rIECSA under flow conditions at 0.05 Pa.

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