Effect of rat andβ-human interferons on hyperacute experimental allergic encephalomyelitis in rats

Hertz, F.; Deghenghi, Romano

doi:10.1007/bf01982879

Cited by 30 publications

(12 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Because nonmethylated B 12 was not effective, the results observed involved biological methylation. Many, but not all, immunological IFN-␤ effects are species specific (34). When hIFN-␤ was used in a similar set of experiments, there was a significant effect of the combination treatment, suggesting that the biological effects relevant in this study were not strictly species specific (data not shown).…”

Section: Combination Therapy Attenuates Nonautoimmune Demyelinationmentioning

confidence: 78%

Attenuation of Experimental Autoimmune Encephalomyelitis and Nonimmune Demyelination by IFN-β plus Vitamin B12: Treatment to Modify Notch-1/Sonic Hedgehog Balance

Mastronardi¹,

Min²,

Wang

et al. 2004

The Journal of Immunology

View full text Add to dashboard Cite

Interferon-β is a mainstay therapy of demyelinating diseases, but its effects are incomplete in human multiple sclerosis and several of its animal models. In this study, we demonstrate dramatic improvements of clinical, histological, and laboratory parameters in in vivo mouse models of demyelinating disease through combination therapy with IFN-β plus vitamin B12 cyanocobalamin {B12CN) in nonautoimmune primary demyelinating ND4 (DM20) transgenics, and in acute and chronic experimental autoimmune encephalomyelitis in SJL mice. Clinical improvement (p values <0.0001) was paralleled by near normal motor function, reduced astrocytosis, and reduced demyelination. IFN-β plus B12CN enhanced in vivo and in vitro oligodendrocyte maturation. In vivo and in vitro altered expression patterns of reduced Notch-1 and enhanced expression of sonic hedgehog and its receptor were consistent with oligodendrocyte maturation and remyelination. IFN-β-B12CN combination therapy may be promising for the treatment of multiple sclerosis.

show abstract

Section: Combination Therapy Attenuates Nonautoimmune Demyelinationmentioning

confidence: 78%

Attenuation of Experimental Autoimmune Encephalomyelitis and Nonimmune Demyelination by IFN-β plus Vitamin B12: Treatment to Modify Notch-1/Sonic Hedgehog Balance

Mastronardi¹,

Min²,

Wang

et al. 2004

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…As discussed above, GA a random copolymer of tyrosine, glutamate, alanine and lysine in ratios resembling myelin basic protein. (Abreu, 1982;Jacobs et al, 1982;Hertz and Deghenghi, 1985;Abreu et al, 1986;Paty and Li, 1993; Brod and Burns, 1994;Ruuls et al, 1996;Yu et al, 1996; Croxford et al, 1998b;van der Meide et al, 1998;Luca et al, 1999;Yasuda et al, 1999;Wender et al, 2001;Schaefer et al, 2006;Jaini et al, 2006;Martin-Saavedra et al, 2007) Other drugs et al, 1971;1973;1974;2004; Keith et al, 1979;Lisak et al, 1983; Aharoni et al, 1993;1997;Johnson et al, 1995;Gran et al, 2000; Gilgun-Sherki et al, 2003;Illes et al, 2004;Stern et al, 2004; Giuliani et al, 2005a,b of the immunogenicity of proteins. GA was developed initially as a putative encephalitogen; however, it showed ...…”

mentioning

confidence: 99%

Experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS)

Constantinescu

Farooqi

O’Brien

et al. 2011

British J Pharmacology

1,218

989

View full text Add to dashboard Cite

Experimental autoimmune encephalomyelitis (EAE) is the most commonly used experimental model for the human inflammatory demyelinating disease, multiple sclerosis (MS). EAE is a complex condition in which the interaction between a variety of immunopathological and neuropathological mechanisms leads to an approximation of the key pathological features of MS: inflammation, demyelination, axonal loss and gliosis. The counter-regulatory mechanisms of resolution of inflammation and remyelination also occur in EAE, which, therefore can also serve as a model for these processes. Moreover, EAE is often used as a model of cell-mediated organ-specific autoimmune conditions in general. EAE has a complex neuropharmacology, and many of the drugs that are in current or imminent use in MS have been developed, tested or validated on the basis of EAE studies. There is great heterogeneity in the susceptibility to the induction, the method of induction and the response to various immunological or neuropharmacological interventions, many of which are reviewed here. This makes EAE a very versatile system to use in translational neuro-and immunopharmacology, but the model needs to be tailored to the scientific question being asked. While creating difficulties and underscoring the inherent weaknesses of this model of MS in straightforward translation from EAE to the human disease, this variability also creates an opportunity to explore multiple facets of the immune and neural mechanisms of immune-mediated neuroinflammation and demyelination as well as intrinsic protective mechanisms. This allows the eventual development and preclinical testing of a wide range of potential therapeutic interventions. LINKED ARTICLESThis article is part of a themed issue on Translational Neuropharmacology. To view the other articles in this issue visit http://dx.doi.org/10. 1111/bph.2011.164.issue-4 Abbreviations ADEM, acute disseminated encephalomyelitis; ADNP, activity dependent neuroprotective protein; AHR, aryl hydrocarbon receptor; APC, antigen-presenting cells; APL, altered peptide ligand; AT, adoptive transfer; C1 and CB2 receptors, cannabinoid receptors 1 and 2; CIS, clinically isolated syndrome; CNS, central nervous system; DA, dark agouti; DMT, disease-modifying treatment; EAE, experimental autoimmune (allergic) encephalomyelitis; EAN, experimental autoimmune (allergic) neuritis; EBV, Epstein-Barr virus; GA, glatiramer acetate; IFN, interferon; IL, interleukin; IL-1RA, interleukin 1 receptor antagonist; JCV, John Cunningham virus; MBP, myelin basic protein; MOG, myelin oligodendrocyte glycoprotein; MRI, magnetic resonance imaging; MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; NABT, normal appearing brain tissue; NAWM, normal appearing white matter; NMO, neuromyelitis optica; NK1 receptor, neurokinin 1 receptor; PGE, prostaglandin E; PLP, proteolipid protein; PP, primary progressive; PR, progressive relapsing; ROR, retinoid orphan receptor; RR, relapsing-remitting; SP, secondary progressive; TCR, T-cell receptor; TGF, transforming growth...

show abstract

“…would be contributing to the increased variance. As far as we know, our findings are the first demonstration that human r-IFN β-1b is efficacious in an animal EAE model, while it failed to suppress in the rat EAE model in contrast to rat IFN β effective (Hertz & Deghenghi, 1985). Since mononuclear cells were markedly less infiltrated into the brain parenchyma by chronic treatment with GPA-Betaferon (preliminary data), it is conceivable that the antigen specific T-cells and activated macrophages are suppressed for their migration into the brain in association with BBB damage (Swanborg, 1995).…”

Section: Discussionmentioning

confidence: 61%

“…An immune-mediated attack on the oligodendrocytes that synthesize MBP is made by the Th 1 cells and the tissue macrophages/microglias that become activated through Th 1 cell cytokine action, mediating demyelination (Cantorna et al, 1996). The onset of clinical signs in the guinea pig model appears in a similar period of time for rats and mice; 6-12 days, [6-7 days reported by Hertz and Deghenghi (1985), 9-12 days by van der Meide et al (1998) and 10 days by Cantorna et al (1996)] after immunization. Hind limbs paralysis was also defined as a major sign in the rodent's model as well.…”

Section: Discussionmentioning

confidence: 91%

“…In correspondence with the human results, "murine IFN β", which is not the same as the cytokine drug employed in humans, can alleviate experimental autoimmune encephalomyelitis (EAE) (Yu et al, 1996), an inflammatory condition in animals that bears similarities to MS. Human IFN beta, to the contrary, had no effect in the rat EAE model, while "rat IFN β" was active in reducing the severity of clinical symptoms of paralysis (Hertz & Deghenghi, 1985). Thus, the animal studies in vivo would make the interpretation more difficult, inasmuch as human-derived cytokines are used in conditions without evidence for corresponding sensitivity of animal cells/tissues to them.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of human recombinant-interferon β in experimental autoimmune encephalomyelitis in guinea pigs

Aritake¹,

Koh

Inoue

et al. 2010

Pharmaceutical Biology

View full text Add to dashboard Cite

Effect of rat andβ-human interferons on hyperacute experimental allergic encephalomyelitis in rats

Cited by 30 publications

References 28 publications

Attenuation of Experimental Autoimmune Encephalomyelitis and Nonimmune Demyelination by IFN-β plus Vitamin B12: Treatment to Modify Notch-1/Sonic Hedgehog Balance

Attenuation of Experimental Autoimmune Encephalomyelitis and Nonimmune Demyelination by IFN-β plus Vitamin B12: Treatment to Modify Notch-1/Sonic Hedgehog Balance

Experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS)

Effects of human recombinant-interferon β in experimental autoimmune encephalomyelitis in guinea pigs

Contact Info

Product

Resources

About