1: Autoimmun Rev. 2005 Apr;4(4):247-52. Epub 2004 Dec 14. 

Enhancement of autoantibody pathogenicity by viral infections in mouse models of
anemia and thrombocytopenia.

Musaji A, Meite M, Detalle L, Franquin S, Cormont F, Preat V, Izui S, Coutelier
JP.

Unit of Experimental Medicine, Institute for Cellular and Molecular Pathology,
Universite catholique de Louvain, Av. Hippocrate 7430, B-1200 Bruxelles,
Belgium.

Viral infections are involved in the pathogenesis of blood autoimmune diseases
such as hemolytic anemia and thrombocytopenia. Although antigenic mimicry has
been proposed as a major mechanism by which viruses could trigger the
development of such diseases, it is not easy to understand how widely different
viruses might induce these blood autoimmune diseases by this sole mechanism. In
mice infected with lactate dehydrogenase-elevating virus (LDV), or mouse
hepatitis virus, and treated with anti-erythrocyte or anti-platelet monoclonal
autoantibodies at a dose insufficient to induce clinical disease by themselves,
the infection sharply enhances the pathogenicity of autoantibodies, leading to
severe anemia or thrombocytopenia. This effect is observed only with antibodies
that induce disease through phagocytosis. Moreover, the phagocytic activity of
macrophages from infected mice is increased and the enhancing effect of
infection on autoantibody-mediated pathogenicity is strongly suppressed by
treatment of mice with clodronate-containing liposomes. Finally, the disease
induced by LDV after administration of autoantibodies is largely suppressed in
animals deficient for gamma-interferon receptor. Together, these observations
suggest that viruses may trigger autoantibody-mediated anemia or
thrombocytopenia by activating macrophages through gamma-interferon production,
a mechanism that may account for the pathogenic similarities of multiple
infectious agents.

PMID: 15893720 [PubMed - in process]