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. 2017 Jul 5;16:279. doi: 10.1186/s12936-017-1930-9

Fig. 3.

Fig. 3

a Inhibition of ItG binding to TNF-stimulated HUVEC under static conditions observed after pre-incubation with 5 µg/ml αICAM-1 mAb for 1 h. b Inhibition of C24 to TNF-stimulated HDMEC under static conditions observed after incubation with 10 µg/ml αCD36 mAb for 1 h. c Inhibition of ItG binding to TNF-stimulated HDMEC under static conditions observed after incubation with 5 µg/ml αICAM-1 and 10 µg/ml αCD36 mAbs independently and the combination of both mAbs, for 1 h. d Reversal of ItG binding to TNF-stimulated HUVEC under static conditions. pRBC were allowed to bind to the cells for 1 h and binding was observed after incubation with 5 µg/ml αICAM-1 mAb for 1 h. e Reversal of C24 binding to TNF stimulated HDMEC under static conditions observed after incubation with 10 µg/ml αCD36 mAb for 1 h. f Reversal of ItG binding to TNF-stimulated HDMEC under static conditions observed after incubation with 5 µg/ml αICAM-1 mAb and 10 µg/ml αCD36 mAb or the combination of these mAbs, for 1 h. Results expressed as mean bound pRBC/mm2 ± standard deviation. Control, without antibody