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HFcγRIIA-expressing platelets are sufficient to induce anaphylaxis in resistant mice. hFcγRIIA-expressing platelets are sufficient to induce anaphylaxis.

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Presentation on theme: "HFcγRIIA-expressing platelets are sufficient to induce anaphylaxis in resistant mice. hFcγRIIA-expressing platelets are sufficient to induce anaphylaxis."— Presentation transcript:

1 hFcγRIIA-expressing platelets are sufficient to induce anaphylaxis in resistant mice.
hFcγRIIA-expressing platelets are sufficient to induce anaphylaxis in resistant mice. (A) Maximal aggregation (%) of washed platelets from hFcγRIIAtg mice compared with baseline and (B) expression of platelet activation markers after incubation with indicated agonist. Data are pooled from three independent experiments. NS, not stimulated. (C to F) hFcγRIIAtg (circles) and FcγRnull (squares) mice were challenged or not with HA-hIgG (n = 4). (C and D) ΔGeoMean CD62P expression (C) on single platelets and (D) within platelet-neutrophil aggregates, (E) percentage of neutrophils associated to CD41+ platelets, and (F) ΔGeoMean CD62L expression on single neutrophils. PSA, passive systemic anaphylaxis. (G and H) Indicated groups of mice were pretreated with anti-CD62P mAb or isotype control (black circles, n = 4) and challenged or not with HA-hIgG (all groups, n = 4). (G) Percentage of neutrophils associated to CD41+ platelets 30 min after challenge and (H) changes in body temperature over time. (I) Washed platelets from hFcγRIIAtg mice (red squares, left) or from FcγRnull mice (gray squares, right), or Tyrode’s albumin buffer (TyAlb) alone (open squares), were transferred intravenously into FcγRnull mice before challenge with HA-hIgG (all groups, n = 3). hFcγRIIAtg mice receiving intravenous injection of TyAlb, followed by challenge with HA-hIgG, served as a positive control (open circles, n = 5). wPLA, washed platelets. Changes in body temperature were recorded. (C to I) Data are representative of at least two independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < Héloïse Beutier et al. Sci. Immunol. 2018;3:eaan5997 Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works


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