Publication Date:
2014-05-02
Description:
Platelets play crucial functions in hemostasis and the prevention of bleeding. During H 1 N 1 influenza A virus infection, platelets display activation markers. The platelet activation triggers during H 1 N 1 infection remain elusive. We observed that H 1 N 1 induces surface receptor activation, lipid mediator synthesis, and release of microparticles from platelets. These activation processes require the presence of serum/plasma, pointing to the contribution of soluble factor(s). Considering that immune complexes in the H 1 N 1 pandemic were reported to play a pathogenic role, we assessed their contribution in H 1 N 1 -induced platelet activation. In influenza-immunized subjects, we observed that the virus scaffolds with immunoglobulin G (IgG) to form immune complexes that promote platelet activation. Mechanistically, this activation occurs through stimulation of low-affinity type 2 receptor for Fc portion of IgG (FcRIIA), a receptor for immune complexes, independently of thrombin. Using a combination of in vitro and in vivo approaches, we found that the antibodies from H 3 N 2 -immunized mice activate transgenic mouse platelets that express FcRIIA when put in the presence of H 1 N 1 , suggesting that cross-reacting influenza antibodies suffice. Alternatively, H 1 N 1 can activate platelets via thrombin formation, independently of complement and FcRIIA. These observations identify both the adaptive immune response and the innate response against pathogens as 2 intertwined processes that activate platelets during influenza infections.
Keywords:
Immunobiology, Platelets and Thrombopoiesis, Thrombosis and Hemostasis
Print ISSN:
0006-4971
Electronic ISSN:
1528-0020
Topics:
Biology
,
Medicine
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