Figure 3
Figure 3. P- and E-selectin ligand expression on neutrophils in St3gal4-deficient, St3gal6-deficient, and double-deficient mice. (A) P- and E-selectin–Ig chimera binding to circulating Gr-1+ leukocytes was analyzed by flow cytometry. Loss of P- and E-selectin–Ig chimera binding in the presence of EDTA is also shown as a control. (B) ECA, RCA, Maackie amurensis lectin, and PNA lectin binding to circulating Gr-1+ cells was assessed by flow cytometry. (C) Expression of leukocyte adhesion molecules (PSGL-1/CD162, CD62L, CD24, CD18, CD11a, and CD11b) was analyzed by flow cytometry. Mean fluorescence intensity is indicated in each histogram and data are representative of 3 independent experiments.

P- and E-selectin ligand expression on neutrophils in St3gal4-deficient, St3gal6-deficient, and double-deficient mice. (A) P- and E-selectin–Ig chimera binding to circulating Gr-1+ leukocytes was analyzed by flow cytometry. Loss of P- and E-selectin–Ig chimera binding in the presence of EDTA is also shown as a control. (B) ECA, RCA, Maackie amurensis lectin, and PNA lectin binding to circulating Gr-1+ cells was assessed by flow cytometry. (C) Expression of leukocyte adhesion molecules (PSGL-1/CD162, CD62L, CD24, CD18, CD11a, and CD11b) was analyzed by flow cytometry. Mean fluorescence intensity is indicated in each histogram and data are representative of 3 independent experiments.

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