Treatment with Anti-interferon-γ Monoclonal Antibodies Modifies Experimental Autoimmune Encephalomyelitis in Interferon-γ Receptor Knockout Mice

Espejo, Carmen; Penkowa, Milena; Sáez-Torres, Irene; Xaus, Jordi; Celada, Antonio; Montalbán, Xavier; Martı́nez-Cáceres, Eva Ma

doi:10.1006/exnr.2001.7815

Cited by 33 publications

(17 citation statements)

References 33 publications

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“…In the previous work, eyes were treated with IFN(s) before viral infection. Therefore, the data for type II IFN-mediated resistance may be based upon either supraphysiologic levels of this cytokine or potential effects that are independent of the type II IFN receptor (12). Nevertheless, our data agree with their conclusions that complementary effects of both types of IFN (41) are needed for host immunity to acute HSV-1 infection.…”

Section: Discussionsupporting

confidence: 84%

Bioluminescence Imaging Reveals Systemic Dissemination of Herpes Simplex Virus Type 1 in the Absence of Interferon Receptors

Luker

Prior

Song

et al. 2003

J Virol

112

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Herpes simplex virus type 1 (HSV-1) can produce disseminated, systemic infection in neonates and patients with AIDS or other immunocompromising diseases, resulting in significant morbidity and mortality in spite of antiviral therapy. Components of host immunity that normally limit HSV-1 to localized epithelial and neuronal infection remain incompletely defined. We used in vivo bioluminescence imaging to determine effects of type I and II interferons (IFNs) on replication and tropism of HSV-1 infection in mice with genetic deficiency of type I, type II, or both type I and II IFN receptors. Following footpad or ocular infection of mice lacking type I IFN receptors, HSV-1 spread to parenchymal organs, including lung, liver, spleen, and regional lymph nodes, but mice survived. Deletion of type I and II IFN receptors produced quantitatively greatest and most widespread dissemination of virus to visceral organs and the nervous system, and these mice invariably died after ocular or footpad infection. Type II receptor knockout and wild-type mice had comparable viral replication and localization, with no systemic spread of HSV-1 or lethality. Therefore, while isolated deficiency of type II IFN receptors did not affect pathogenesis, loss of these receptors in combination with genetic deletion of type I receptors had a profound effect on susceptibility to HSV-1. These data demonstrate different effects of type I and II IFNs in limiting systemic dissemination of HSV-1 and further validate the use of bioluminescence imaging for studies of viral pathogenesis.

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Section: Discussionsupporting

confidence: 84%

Bioluminescence Imaging Reveals Systemic Dissemination of Herpes Simplex Virus Type 1 in the Absence of Interferon Receptors

Luker

Prior

Song

et al. 2003

J Virol

112

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“…Potentiation of the biological activity of cytokines by antibody anti-cytokines has been described for IL-2, IL-3, IL-6, IFN-␥, and TNF. [41][42][43][44][45] This phenomenon has been associated with formation of stable complexes between cytokines and their respective antibodies that optimize the immune response. 41 It is probable that decreased parasite load after using anti-MIF antibody may be associated with formation of complexes between anti-MIF and endogenous MIF that potentiated the MIF effect.…”

Section: Discussionmentioning

confidence: 99%

Effect of Macrophage Migration Inhibitory Factor (MIF) in Human Placental Explants Infected with Toxoplasma gondii Depends on Gestational Age

Gomes¹,

Silva²,

Silva³

et al. 2011

The American Journal of Pathology

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Because macrophage migration inhibitory factor (MIF) is a key cytokine in pregnancy and has a role in inflammatory response and pathogen defense, the objective of the present study was to investigate the effects of MIF in first-and third-trimester human placental explants infected with Toxoplasma gondii. Explants were treated with recombinant MIF, IL-12, interferon-␥, transforming growth factor-␤1, or IL-10, followed by infection with T. gondii RH strain tachyzoites. Supernatants of cultured explants were assessed for MIF production. Explants were processed for morphologic analysis, immunohistochemistry, and real-time PCR analysis. Comparison of infected and stimulated explants versus noninfected control explants demonstrated a significant increase in MIF release in first-trimester but not third-trimester explants. Tissue parasitism was higher in third-than in first-trimester explants. Moreover, T. gondii DNA content was lower in first-trimester explants treated with MIF compared with untreated explants. However, in third-trimester explants, MIF stimulus decreased T. gondii DNA content only at the highest concentration of the cytokine. In addition, high expression of MIF receptor was observed in first-trimester placental explants, whereas MIF receptor expression was low in third-trimester explants. In conclusion, MIF was up-regulated and demonstrated to be important for control of T. gondii infection in first-trimester explants, whereas lack of MIF up-regulation in third-trimester placentas may be involved in higher susceptibility to infection at this gestational age.

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“…13 However, it is unclear whether the increased IFNg expression is a deleterious or a disease limiting response in EAE, as IFNg receptor knockout mice are more susceptible to EAE than wild-type mice. 14,15 Transgenic mice overexpressing IFNg in the central nervous system under the control of an oligodendrocyte-specific promoter develop extensive primary demyelination compared to wild-type mice. 16,17 IFNg may exert deleterious effects directly on myelinating cells and also through activation of macrophages and microglia.…”

Section: Introductionmentioning

confidence: 99%

IFNG polymorphisms are associated with gender differences in susceptibility to multiple sclerosis

et al. 2005

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Interferon-gamma (IFNg) treatment is deleterious in multiple sclerosis (MS). MS occurs twice as frequently in women as in men. IFNg expression varies by gender. We studied a population-based sample of US MS patients and ethnicity-matched controls and independent Northern Irish and Belgian hospital-based patients and controls for association with MS, stratified by gender, of an intron 1 microsatellite [I1 (761)

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Treatment with Anti-interferon-γ Monoclonal Antibodies Modifies Experimental Autoimmune Encephalomyelitis in Interferon-γ Receptor Knockout Mice

Cited by 33 publications

References 33 publications

Bioluminescence Imaging Reveals Systemic Dissemination of Herpes Simplex Virus Type 1 in the Absence of Interferon Receptors

Bioluminescence Imaging Reveals Systemic Dissemination of Herpes Simplex Virus Type 1 in the Absence of Interferon Receptors

Effect of Macrophage Migration Inhibitory Factor (MIF) in Human Placental Explants Infected with Toxoplasma gondii Depends on Gestational Age

IFNG polymorphisms are associated with gender differences in susceptibility to multiple sclerosis

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