Ameliorating Effect of IFN-β and Anti-IFN-β on Coxsackievirus B3-Induced Myocarditis in Mice

Lutton, C. William; Gauntt, Charles J.

doi:10.1089/jir.1985.5.137

Cited by 59 publications

(29 citation statements)

References 36 publications

(5 reference statements)

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“…This may be due to inhibition of IFN and gp130 signaling. The induction of SOCS1 and SOCS3 on day 3 after infection may explain the fact that IFN administration is only beneficial in CVB3-induced myocarditis when given early (22). Our data do not exclude the possibility that SOCS expression may be beneficial in late stages of infection or in other disease states that activate JAK-STAT signaling in the heart.…”

Section: Discussionmentioning

confidence: 60%

“…It has been shown that administration of IFN-α or -β can have a beneficial effect on viral myocarditis in the early stages of infection (22), but whole-animal knockouts of the IFN-α/β receptor had no detectable effect on the extent of viral infection in the heart during the early stages of infection in spite of a marked effect on viral replication in the liver (23). Furthermore, little is known regarding the effect of JAK-STAT activation by other cytokines, such as CT-1 and IL-6, in viral heart disease.…”

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confidence: 99%

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The suppressor of cytokine signaling–1 (SOCS1) is a novel therapeutic target for enterovirus-induced cardiac injury

Yasukawa¹,

Yajima²,

Duplain³

et al. 2003

J. Clin. Invest.

112

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Section: Discussionmentioning

confidence: 60%

mentioning

confidence: 99%

The suppressor of cytokine signaling–1 (SOCS1) is a novel therapeutic target for enterovirus-induced cardiac injury

Yasukawa¹,

Yajima²,

Duplain³

et al. 2003

J. Clin. Invest.

112

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“…Recent work with Coxsaclde B3-induced myocarditis has shown that administration of interferon or poly I:C could protect against these virus-induced lesions only if they were given within 24 h of virus infection or concomitantly. Administration of interferon at 72 h, rather than protecting as it did earlier, accelerated the development of myocardial lesions [28]. These workers suggest that interferon may play different roles in the viral infection, depending upon the time of administration.…”

Section: Treatmentmentioning

confidence: 97%

Factors affecting the infection of the D variant of encephalomyocarditis virus in the B cells of C57BL/6J mice

1987

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Summary. The D variant of encephalomyocarditis virus is capable of infecting most inbred strains of mice. However, only certain strains are susceptible to the diabetogenic effect of this virus. In order to understand why some inbred strains do not become diabetic, the pathogenesis of infection was studied in diabetes-resistant C57BL/6J mice. It was the purpose of the investigation to ascertain whether specific host defense factors might play a crucial role in the mechanism of resistance. To determine whether perturbations of the immune response would alter the resistance of these animals, mice were treated with a high dose (1.15 mmol/kg body weight) of the T-and B-cell toxin cyclophosphamide prior to infection with the D variant. This treatment did not induce overt diabetes or glucose intolerance in the mice tested 7 days after infection. Based on this finding, it appeared likely that resistance to the D variant is conveyed by some factor other than cell-mediated immunity. A likely candidate to control this viral infection is the interferon system. To investigate this possibility, C57BL/6J mice were infected with the D variant and the concentrations of serum interferon titred at various intervals thereafter. In contrast to previous reports with diabetes susceptible mice, C57BL/6J mice were found to generate a substantial interferon response against this variant, with peak levels found in the serum at 24 h following infection. Additional studies were performed in which mice were treated with antibody to mouse interferon alpha/beta at the time of infection and again 3 days after infection with the D variant. Sixty percent of the animals treated in this manner became glucose intolerant. The results of these studies indicate that the interferon system is a critical determinant of resistance to the diabetogenic effect of the D variant in C57BL/6J mice.Key words: D variant of encephalomyocarditis virus, C57BL/ 6J mice, interferon response, B cell destruction, cyclophosphamide treatment.A viral etiology for Type 1 (insulin-dependent) diabetes mellitus has been suggested by the abrupt onset of clinical symptoms and seasonal variations sometimes seen in this disease [1]. The description of a murine model for Type I diabetes induced by encephalomyocarditis virus (EMCV) provided a means for examining experimentally the possible role of viruses in this disease [2][3][4][5]. Two strains of EMCV were initially isolated -an E strain that is highly neurotropic, and a M strain that produces myocarditis and little central nervous system involvement [6]. This M strain is capable of inducing a diabetes mellitus-like disease by the selective destruction of pancreatic B cells in certain inbred strains of mice [4]. Other inbred strains of mice are resistant to this diabetogenic effect, even though these animals sustain a viral infection. Further investigations into the M strain resulted in the isolation of two variants -a B variant which is nondiabetogenic, and a D variant which causes this disease [7]. Although strains of mice have b...

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“…Viral replication in cardiomyocytes leads to induction of cytokines including ␣ and ␤-interferons which are important antiviral cytokines which inhibit viral replication. 23,24 In the early acute phase of myocarditis, the virus reacts with toll-like receptor(TLR) 4 which signals danger in the heart. 25,26 The response to TLR4 signaling includes the induction of inflammatory cytokines.…”

mentioning

confidence: 99%

T Regulatory Cells

Cunningham

2006

Circulation Research

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Ameliorating Effect of IFN-β and Anti-IFN-β on Coxsackievirus B3-Induced Myocarditis in Mice

Cited by 59 publications

References 36 publications

The suppressor of cytokine signaling–1 (SOCS1) is a novel therapeutic target for enterovirus-induced cardiac injury

The suppressor of cytokine signaling–1 (SOCS1) is a novel therapeutic target for enterovirus-induced cardiac injury

Factors affecting the infection of the D variant of encephalomyocarditis virus in the B cells of C57BL/6J mice

T Regulatory Cells

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