Acute Infection of Mice with Lactate Dehydrogenase-elevating Virus Enhances Fc and Complement Receptor Activity of Peritoneal Macrophages

Lussenhop, Nancy; Holmes, Beulah; Cafruny, William A.; Plagemann, Peter G.W.

doi:10.1099/0022-1317-61-1-25

Cited by 26 publications

(10 citation statements)

References 32 publications

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“…Although many viral infections result in a decrease in macrophage functions, including phagocytosis, some viruses, such as herpes simplex virus (2), Coxsackie virus (22), or Newcastle disease virus (19), have been shown to enhance the ability of these cells to incorporate various targets. Whereas contradictory results have been reported after LDV infection (17,18,32), another nidovirus, mouse hepatitis virus, can also increase macrophage-mediated phagocytosis (33).…”

Section: Discussionmentioning

confidence: 99%

Exacerbation of Autoantibody-Mediated Hemolytic Anemia by Viral Infection

Meité

Léonard

Idrissi

et al. 2000

J Virol

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Strong enhancement of the pathogenicity of an antierythrocyte monoclonal antibody was observed after infection of mice with lactate dehydrogenase-elevating virus. While injection of the antierythrocyte antibody alone induced only moderate anemia, concomitant infection with this virus, which is harmless in most normal mice, led to a dramatic drop in the hematocrit and to death of infected animals. In vitro and in vivo analyses showed a dramatic increase in the ability of macrophages from infected mice to phagocytose antibody-coated erythrocytes. These results indicate that viruses can trigger the onset of autoimmune disease by enhancing the pathogenicity of autoantibodies. They may explain how unrelated viruses could be implicated in the etiology of autoantibody-mediated autoimmune diseases.A causal connection between viral infection and the development of clinical pathology has long been suspected for a number of autoimmune diseases mediated by autoantibodies (reviewed in reference 36). Interestingly, in most cases, several different viruses have been proposed as etiologic agents of the same disease. Experimental data have suggested that viruses trigger an autoimmune humoral response by distinct mechanisms, including polyclonal B-lymphocyte activation, antigenic mimicry, modification of self-antigen, production of anti-idiotypic antibodies, or enhancement of major histocompatibility complex molecule expression on potential antigen-presenting cells (4,9,11,15,20,25,31,37). However, although it has been conclusively shown in several models that autoantibody secretion was triggered by infection, the actual pathogenicity of these antibodies has not always been demonstrated. Similarly, other stimuli, like immunization of mice with rat red blood cells, may lead to autoantibody production without development of the corresponding disease, in this case, hemolytic anemia (8,24,34). Therefore, it may be that mere autoantibody secretion is not sufficient to trigger an autoimmune disease and that the immune environment of the host plays an important role in the pathogenicity of such autoantibodies.Viruses have also been shown to variably affect macrophage functions, including cytokine production and the ability to present antigens (6, 16). Since it is known that some autoantibody-mediated diseases involve phagocytosis by macrophages, we postulated that modulation of this cellular function may explain the induction of such clinical diseases observed in the course of viral infections. To test this hypothesis, we used an experimental model of anemia induced by administration of antierythrocyte monoclonal antibodies (29). Our results indicate that a viral infection with lactate dehydrogenase-elevating virus (LDV) may trigger a dramatic hemolytic disease by enhancing the pathogenicity of autoantibodies. If confirmed with other models, this observation may indicate how different viruses can trigger similar clinical autoimmune diseases and open the way to novel therapeutic approaches. MATERIALS AND METHODSMice. Female BALB/c mice w...

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Section: Discussionmentioning

confidence: 99%

Exacerbation of Autoantibody-Mediated Hemolytic Anemia by Viral Infection

Meité

Léonard

Idrissi

et al. 2000

J Virol

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“…Herpes simplex virus type 1 and cytomegalovirus induce formation of a virus glycoprotein which acts as Fc-receptor, even on non-phagocytic cells (Westmoreland & Watkins, 1974;Keller et al, 1976;Westmoreland et al, 1976;Para et al, 1980). Another mechanism is mediated by interferon, as seen in lactate dehydrogenase-elevating virus and Newcastle disease virus infection of mice (Hamburg et al, 1978;Lussenhop et al, 1982). There is no evidence that dengue virus is a good inducer of interferon.…”

Section: Discussionmentioning

confidence: 99%

Effect of Dengue Virus Infection on Fc-receptor Functions of Mouse Macrophages

Chaturvedi¹,

Nagar²,

Mathur³

1983

Journal of General Virology

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“…IFN-a/p is only transiently detected in infected mice 1-day postinfection (Rowson and Mahy, 1985). It is probably produced by the large number of LDV-permissive macrophages that become productively infected during the primary infection of a mouse (Lussenhop et al, 1982). Macrophages that become infected during the subsequent persistent phase of infection probably also produce IFN-a/& but since their numbers are relatively small, the plasma concentration of IFN-aIP remains below detectable levels.…”

Section: Anti-ldv Immune Responses a Polyclonal Anti-ldv Responses Dmentioning

confidence: 99%