Figure 1
Figure 1. FcγRIIB, but not FcγRIII, mediates anti–GPVI-induced thrombocytopenia and the generation of sGPVI. (A) Platelet counts of 2.4G2 (gray) or vehicle-treated (black) mice were monitored upon injection of the anti-GPVI antibody JAQ1biotin by flow cytometry. (B) Expression of GPVI on the platelet surface was determined by flow cytometry using an anti-rat IgG-fluorescein isothiocyanate (FITC) antibody. (C) Plasma levels of sGPVI) were determined using an enzyme-linked immunosorbent assay (ELISA) system. (D) Platelet counts of mice lacking FcγRIII (Fcgr3−/−), FcγRIIB (Fcgr2b−/−), or control mice (WT) were monitored upon injection of the anti-GPVI antibody JAQ1biotin by flow cytometry. (E) Expression of GPVI on the platelet surface was determined by flow cytometry using an anti-rat IgG-FITC antibody. (F) Plasma levels of soluble GPVI (sGPVI) were determined using an ELISA system. Data are expressed as mean ± standard deviation (n = 4) and are representative of 3 individual experiments.

FcγRIIB, but not FcγRIII, mediates anti–GPVI-induced thrombocytopenia and the generation of sGPVI. (A) Platelet counts of 2.4G2 (gray) or vehicle-treated (black) mice were monitored upon injection of the anti-GPVI antibody JAQ1biotin by flow cytometry. (B) Expression of GPVI on the platelet surface was determined by flow cytometry using an anti-rat IgG-fluorescein isothiocyanate (FITC) antibody. (C) Plasma levels of sGPVI) were determined using an enzyme-linked immunosorbent assay (ELISA) system. (D) Platelet counts of mice lacking FcγRIII (Fcgr3−/−), FcγRIIB (Fcgr2b−/−), or control mice (WT) were monitored upon injection of the anti-GPVI antibody JAQ1biotin by flow cytometry. (E) Expression of GPVI on the platelet surface was determined by flow cytometry using an anti-rat IgG-FITC antibody. (F) Plasma levels of soluble GPVI (sGPVI) were determined using an ELISA system. Data are expressed as mean ± standard deviation (n = 4) and are representative of 3 individual experiments.

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