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Exacerbation of autoantibody-mediated thrombocytopenic purpura by infection with mouse viruses
Andrei Musaji1, Françoise Cormont, Gaëtan Thirion
1Unit of Experimental Medicine, Institute for Cellular Pathology, Université Catholique de Louvain, Brussels, Belgium.
Abstract:
Antigenic mimicry has been proposed as a major mechanism by which viruses could trigger the development of immune thrombocytopenic purpura (ITP). However, because antigenic mimicry implies epitope similarities between viral and self antigens, it is difficult to understand how widely different viruses can be involved by this sole mechanism in the pathogenesis of ITP. Here, we report that in mice treated with antiplatelet antibodies at a dose insufficient to induce clinical disease by themselves, infection with lactate dehydrogenase-elevating virus (LDV) was followed by severe thrombocytopenia and by the appearance of petechiae similar to those observed in patients with ITP. A similar exacerbation of antiplatelet-mediated thrombocytopenia was induced by mouse hepatitis virus. This enhancement of antiplatelet antibody pathogenicity by LDV was not observed with F(ab')2 fragments, suggesting that phagocytosis was involved in platelet destruction. Treatment of mice with clodronate-containing liposomes and with total immunoglobulin G (IgG) indicated that platelets were cleared by macrophages. The increase of thrombocytopenia triggered by LDV after administration of antiplatelet antibodies was largely suppressed in animals deficient for gamma-interferon receptor. Together, these results suggest that viruses may exacerbate autoantibody-mediated ITP by activating macrophages through gamma-interferon production, a mechanism that may account for the pathogenic similarities of multiple infectious agents.
Insights
Viruses can worsen immune thrombocytopenic purpura (ITP) by activating macrophages. This gamma-interferon dependent mechanism explains how diverse viruses contribute to ITP pathogenesis.
Area of Science:
- Immunology
- Virology
- Pathogenesis of ITP
Background:
- Antigenic mimicry is a proposed mechanism for viral-induced immune thrombocytopenic purpura (ITP).
- The mechanism struggles to explain how diverse viruses contribute to ITP pathogenesis.
- This study investigates alternative viral roles in ITP development.
Purpose of the Study:
- To elucidate the mechanism by which viruses exacerbate antiplatelet antibody-induced thrombocytopenia.
- To determine the role of macrophage phagocytosis and gamma-interferon in viral exacerbation of ITP.
Main Methods:
- Mice were treated with sub-clinical doses of antiplatelet antibodies and infected with lactate dehydrogenase-elevating virus (LDV) or mouse hepatitis virus.
- Phagocytosis was assessed using F(ab')2 fragments.
- Macrophage activity was inhibited using clodronate liposomes and total IgG.
- The role of gamma-interferon was evaluated in deficient mice.
Main Results:
- LDV and mouse hepatitis virus infection exacerbated antiplatelet antibody-induced thrombocytopenia.
- Enhanced thrombocytopenia was dependent on Fc-mediated phagocytosis, implicating macrophages.
- Macrophage clearance of platelets was confirmed.
- Viral exacerbation of thrombocytopenia was significantly reduced in gamma-interferon receptor-deficient mice.
Conclusions:
- Viruses can exacerbate autoantibody-mediated ITP through macrophage activation.
- Gamma-interferon production by immune cells is a key mediator of this exacerbation.
- This mechanism provides a unifying explanation for the involvement of diverse viruses in ITP pathogenesis.
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