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. 2022 Mar 7;59(2):89–96. doi: 10.1053/j.seminhematol.2022.03.002

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Fig. 2 — Inhibition of platelet activation by high-dose IVIG. Platelet activation (as shown by percent serotonin-release) in the standard serotonin-release assay (SRA) (leftmost panel) and in the PF4-enhanced SRA (PF4-SRA; rightmost panel) for serial samples obtained for 3 patients—samples obtained before and after 2 to 4 doses of high-dose intravenous immune globulin (IVIG). In all 3 patients, samples obtained post-IVIG showed substantial decrease in serum-induced platelet activation. In contrast, there was no inhibition of EIA reactivity, shown as units of optical density (OD); boxed insets in leftmost panel). These data indicate that IVIG works by inhibiting platelet activation through platelet FcγIIa receptors, rather than by inhibiting interaction between the antibodies and the antigen target(s) on PF4. Reprinted (with modifications) [24] with permission of the Massachusetts Medical Society. EIA, enzyme-immunoassay; IV.3 indicates an Fc receptor-blocking monoclonal antibody; IVIG, intravenous immune globulin; OD, optical density; PF4, platelet factor 4; U, units.