Fig. 4.
Fig. 4. Adhesion of hemopoietic cells to ICAM4Fc is not αLβ2-mediated. / Adhesion assays were as described in “Materials and methods.” Results are input cells bound ± SD (n = 6). (A) Adhesion of cation-activated HEL cells to ICAM-4 and mutant ICAM-4–Fc proteins (coated at 0.5 μg/well). (B) Binding of PMA+ cation–activated THP1 cells to ICAM-1–Fc, -2–Fc, and -3–Fc, ICAM4Fc, and mutant ICAM-4–Fc proteins (coated at 0.5 μg/well) in the presence of inhibiting anti-αL (mab 38, hatched), anti-β2 (1B4, black) antibodies or a control antibody (white). (C) Adhesion of PMA+ cation–activated IM9 cells to ICAMs–Fc, -2–Fc, and -3–Fc, ICAM4Fc, and mutant ICAM4Fc proteins (coated at 1 μg/well). Cells were treated with either control antibody (white) or activating β2antibodies, KIM127 (hatched) or KIM185 (black).

Adhesion of hemopoietic cells to ICAM4Fc is not αLβ2-mediated.

Adhesion assays were as described in “Materials and methods.” Results are input cells bound ± SD (n = 6). (A) Adhesion of cation-activated HEL cells to ICAM-4 and mutant ICAM-4–Fc proteins (coated at 0.5 μg/well). (B) Binding of PMA+ cation–activated THP1 cells to ICAM-1–Fc, -2–Fc, and -3–Fc, ICAM4Fc, and mutant ICAM-4–Fc proteins (coated at 0.5 μg/well) in the presence of inhibiting anti-αL (mab 38, hatched), anti-β2 (1B4, black) antibodies or a control antibody (white). (C) Adhesion of PMA+ cation–activated IM9 cells to ICAMs–Fc, -2–Fc, and -3–Fc, ICAM4Fc, and mutant ICAM4Fc proteins (coated at 1 μg/well). Cells were treated with either control antibody (white) or activating β2antibodies, KIM127 (hatched) or KIM185 (black).

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