| First Author | Legrain S | Year | 2015 |
| Journal | J Immunol | Volume | 195 |
| Issue | 9 | Pages | 4171-5 |
| PubMed ID | 26385523 | Mgi Jnum | J:240097 |
| Mgi Id | MGI:5882382 | Doi | 10.4049/jimmunol.1500798 |
| Citation | Legrain S, et al. (2015) Involvement of Fcalpha/mu Receptor in IgM Anti-Platelet, but Not Anti-Red Blood Cell Autoantibody Pathogenicity in Mice. J Immunol 195(9):4171-5 |
| abstractText | IgM anti-mouse platelet autoantibodies cause thrombocytopenia by mediating uptake of opsonized thrombocytes, whereas IgM anti-erythrocyte autoantibodies induce anemia through a phagocytosis-independent cell destruction. In this article, we show that infection with lactate dehydrogenase-elevating virus, a benign mouse arterivirus, exacerbates the pathogenicity of IgM anti-platelet, but not anti-erythrocyte autoantibodies. To define the role of Fcalpha/mu receptor (Fcalpha/muR) in IgM-mediated thrombocytopenia and anemia, we generated mice deficient for this receptor. These animals were resistant to IgM autoantibody-mediated thrombocytopenia, but not anemia. However, the lactate dehydrogenase-elevating virus-induced exacerbation of thrombocytopenia was not associated with enhanced Fcalpha/muR expression on macrophages. These results indicate that Fcalpha/muR is required for the pathogenicity of IgM anti-platelet autoantibodies but is not sufficient to explain the full extent of the disease in virally infected animals. |
