Skip to main content
. Author manuscript; available in PMC: 2014 Jul 3.
Published in final edited form as: Immunity. 2007 Apr;26(4):477–489. doi: 10.1016/j.immuni.2007.03.011

Figure 2. Contribution of ESL-1, PSGL-1 and CD44 in binding of soluble E-selectin.

Figure 2

Flow cytometric analyses of E-selectin/IgM chimera binding to blood neutrophils obtained from mice transplanted with Lin- cells from wild-type, Cd44−/−, Selplg−/− or DKO donors that were transduced with GFP control or shESL-1 vectors. (A) Representative dot plots showing GFP expression (upper quadrants, green) and E-selectin binding in the control (top panels) or shESL (middle panels) groups. Control binding in the presence of EDTA in untransduced neutrophils was used to set the quadrants. Histograms (bottom panels) show overlays of E-selectin binding to neutrophils from the GFP control (light green) and shESL-1 (dark green) groups, as well as control binding in the presence of EDTA (grey) for each donor group. E-selectin binding was reduced to the levels of EDTA controls in the absence of both PSGL-1 and ESL-1. (B) Quantitative summary of E-selectin binding intensities in all eight groups. Inset shows expanded Eselectin binding for the Selplg−/− and DKO groups. n=6-18 mice per group. * p=0.08, ** p<0.0001 compared to the respective GFP vector controls; #, p<0,0001 compared to WT GFP vector; ‡, p<0.0001 compared to WT or CD44 GFP vector groups. §, p<0.0001 compared to WT or CD44 shESL-1 groups.