Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 16, Pages -Publisher
MDPI
DOI: 10.3390/ijms22169027
Keywords
Fc receptors; lactate dehydrogenase-elevating virus; autoimmune anemia; interferon
Funding
- Fonds National de la Recherche Scientifique (FNRS)
- Actions de recherche concertees from the Communaute francaise de Belgique, Direction de la Recherche Scientifique, Belgium
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Infection with LDV can enhance the phagocytosis of autoantibody-opsonized erythrocytes by macrophages, leading to autoimmune anemia. The presence of interferons can partially regulate the expression of FcγR I and IV, which in turn affects the severity of anemia.
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 Fc gamma receptors (Fc gamma R) I, III, and IV. Whereas LDV infection decreases Fc gamma R III expression, it enhances Fc gamma R I and IV expression in wild-type animals. The LDV-associated increase in the expression of Fc gamma R 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 Fc gamma R 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.
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