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. Author manuscript; available in PMC: 2008 Oct 21.
Published in final edited form as: J Infect Dis. 2008 Jan 1;197(1):72–78. doi: 10.1086/523761

Figure 3. P-selectin expressed by activated platelets acts with CD36 as a major receptor for PRBC clumping.

Figure 3

Platelet activation was measured before and after co-incubation with PRBC. The level of membrane P-selectin expression was assessed by immunofluorescence on slide (A, B) and flow cytometry (C, D, E and F). Micrographs, dotplots and histograms presented here are representative of the results observed for 4 assays. The addition of PRBC resulted in the generation of a platelet-PRBC clump population observed in the dotplot D, and the platelet population non associated with PRBC was sub-gated in [p]. Inhibition assays were then performed to evaluate the role of P-selectin and other several platelet surface molecules in the parasite clumping phenomenon. PRP from healthy donors was incubated with either IgG [control] (10 μg/ml), anti-P-selectin (20μg/ml), anti-CD36 (10 μg/ml), a mixture of both anti-P-selectin and CD36 (stated as ‘mix’), Reopro (30 μg/ml) or Lamifiban (100 ng/ml) before the clumping assays with PRBC from CM patients. Histograms are expressed as mean ± SD of percentage of PRBC that are associated with clumps after 120 min. Mann-Whitney U test was used to compare pairs of groups, and a p value < 0.05 was considered significant. Assays were performed 2 times per CM patient sample.