Interferon β Modulates Experimental Autoimmune Encephalomyelitis by Altering the Pattern of Cytokine Secretion

Yasuda, Clarissa L.; Al‐Sabbagh, Ahmad; Oliveira, E. Capelas de; Diaz-Bardales, Blanca Maria; Garcia, Concilia; Santos, Leonilda M.B.

doi:10.3109/08820139909061141

Cited by 37 publications

(23 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[38][39][40] The different biologic effects of IFN␣ and ␤ are difficult to explain since they bind to the same receptor. One possible explanation is their different affinities for the 2 receptor subunits, leading to qualitative differences in downstream signaling pathways and to differential gene activation.…”

Section: Discussionmentioning

confidence: 99%

Interferon β induces mature dendritic cell apoptosis through caspase-11/caspase-3 activation

Yen

Ganea

2009

Blood

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Interferon β induces mature dendritic cell apoptosis through caspase-11/caspase-3 activation

Yen

Ganea

2009

Blood

View full text Add to dashboard Cite

“…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 ...…”

Section: Ifn-betamentioning

confidence: 99%

“…Yes (licensed, widely used) (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 Captopril, losartan, pentoxyphyline, prazosin, antihistamines, and others…”

Section: Ifn-betamentioning

confidence: 99%

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

Constantinescu

Farooqi

O’Brien

et al. 2011

British J Pharmacology

1,228

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

“…Because the pathogenesis of MS results from excessive function of the immune system, treatment is primarily by a combination of IFN-␤ and immunosuppressants (1,2). IFN-␤ inhibits gelatinase B and matrix metalloproteinase and is thought to improve the disease by inhibiting the migration of T cells to CNS (3)(4)(5). Experimental autoimmune encephalomyelitis (EAE) is an inflammatory demyelinating disease of the CNS that is induced by immunizing laboratory rodents with myelin proteins or peptides emulsified in CFA.…”

Section: Ultiple Sclerosis (Ms)mentioning

confidence: 99%

Highly Oligomeric Procyanidins Ameliorate Experimental Autoimmune Encephalomyelitis via Suppression of Th1 Immunity

Miyake

Sasaki

Ide

et al. 2006

The Journal of Immunology

View full text Add to dashboard Cite

Extracts of Jatoba, a South American herb, when injected i.p. into a mouse model of experimental autoimmune encephalomyelitis (EAE), inhibited the aggravation of clinical symptoms. At the same time, production of myelin oligodendrocyte glycoprotein Ag-specific IFN-γ and TNF-α by spleen cells was markedly suppressed. After administration of Jatoba there was minimal evidence of the demyelination that is characteristic of the EAE model. Decreases in clinical scores were observed when Jatoba extracts were injected just before Ag. The purified active compounds are likely to be polyphenols that are absorbable to polyvinylpolypyrrolidone. The active compounds were polymerized polyphenol polymers (procyanidins) and at least five degrees of polymerization were necessary for activity. In addition, extracts of other plant materials containing such procyanidins had similar activity. After administration of highly polymerized procyanidins, there was a decrease in both dendritic and CD4+ T cells. Although macrophages were increased in number, the expression of CD80 and MHC class II molecules was depressed indicating that the macrophages were immature. The results indicate that the suppression of development of EAE by the highly polymerized procyanidins resulted from an inhibition of Th1 and the effects might be associated with depression of Ag-presenting capability.

show abstract

Interferon β Modulates Experimental Autoimmune Encephalomyelitis by Altering the Pattern of Cytokine Secretion

Cited by 37 publications

References 25 publications

Interferon β induces mature dendritic cell apoptosis through caspase-11/caspase-3 activation

Interferon β induces mature dendritic cell apoptosis through caspase-11/caspase-3 activation

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

Highly Oligomeric Procyanidins Ameliorate Experimental Autoimmune Encephalomyelitis via Suppression of Th1 Immunity

Contact Info

Product

Resources

About