Involvement of Virus-Induced Interferon Production in IgG Autoantibody-Mediated Anemia.

Abstract

Infection with viruses, such as the lactate dehydrogenase-elevating virus (LDV), is known to trigger the onset of autoimmune anemia through the enhancement of the phagocytosis of autoantibody-opsonized erythrocytes by activated macrophages. Type I interferon receptor-deficient mice show enhanced anemia, which suggests a protective effect of these cytokines, partly through the control of type II interferon production. The development of anemia requires the expression of Fcγ receptors (FcγR) I, III, and IV. Whereas LDV infection decreases FcγR III expression, it enhances FcγR I and IV expression in wild-type animals. The LDV-associated increase in the expression of FcγR I and IV is largely reduced in type I interferon receptor-deficient mice, through both type II interferon-dependent and -independent mechanisms. Thus, the regulation of the expression of FcγR I and IV, but not III, by interferons may partly explain the exacerbating effect of LDV infection on anemia that results from the enhanced phagocytosis of IgG autoantibody-opsonized erythrocytes.

• Authors: Sarah Legrain, Dan Su, Mélanie Gaignage, Cor Breukel, Jill Claassens, Conny Brouwers, Margot M Linssen, Shozo Izui, J Sjef Verbeek, Jean-Paul Coutelier
• Journal: International journal of molecular sciences (Int J Mol Sci) Vol. 22 Issue 16 (Aug 21 2021) ISSN: 1422-0067 [Electronic] Switzerland
• PMID: 34445732 (Publication Type: Journal Article)

Chemical References

• Receptors, IgG
• Interferons

Topics

• Anemia, Hemolytic, Autoimmune (immunology, virology)
• Animals
• Arterivirus Infections (immunology, virology)
• Host-Pathogen Interactions
• Interferons (metabolism)
• Lactate dehydrogenase-elevating virus (immunology)
• Mice, Inbred C57BL
• Mice, Knockout
• Phagocytosis
• Receptors, IgG (metabolism)
• Mice