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. Author manuscript; available in PMC: 2013 Dec 27.
Published in final edited form as: Nature. 2013 Jun 5;498(7455):502–505. doi: 10.1038/nature12216

Table 1.

Binding (median units* and 95CI) to human endothelial cells (HBMEC) and transfected CHO cells of parasite lines from patients with severe or mild malaria

Parasites HBMEC binding HBMEC via EPCR§ HBMEC via ICAM1§ CHO-ICAM1$ CHO-CD36$
Severe malaria (N=15) 58 [40;80] 40# [20;50] 27 [8;48] 26 [10;42] 19 [8;34]
Uncomplicated (N=5) Pvalue& 25 [14;34] (P=0.021) 7 [4;19] (P=0.0078) 4 [1;20] (P=0.027) 4 [0;6] (P=0.020) 21 [12;25] (P=0.75)
Mild malaria (N=10) Pvalue% 24 [12;45] (P=0.0039) 8 [4;17] (P=0.0009) 2 [0;6] (P=0.0016) 0 [0;1] (P=0.0008) 10 [2;37] (P=0.39)
*

100 units represent optimal binding defined as the HBMEC binding observed with the IT4 parasite line selected to express IT4VAR20 (Figure 2).

§

HBMEC binding inhibited by incubating parasites in the presence of soluble EPCR (30 ug/ml) or anti-ICAM-1 monoclonal antibody (50 ug/ml) given as delta binding units (HBMEC binding subtracted binding in the presence of soluble EPCR or anti-ICAM1).

$

Binding to Chinese hamster ovary cells (CHO) transfected with ICAM-1 or CD36.

#

Among parasites from patients with severe disease EPCR binding statistically significantly higher (Wilcoxon test for paired data) than HBMEC ICAM-1 binding (P=0.01) or binding to CHO-ICAM1 (P<0.05).

%

Wilcoxon rank sum test for comparison between parasites from the two patients groups.