All-trans Retinoic Acid Potentiates the Ability of Interferon Beta-1b to Augment Suppressor Cell Function in Multiple Sclerosis

Qu, Zhi; Dayal, Amit; Jensen, Mark A.; Arnason, Barry G. W.

doi:10.1001/archneur.55.3.315

Cited by 36 publications

(20 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the longitudinal study, the use of interferon-β did not influence our results. In studies by others on this topic conflicting results have been found: some found a synergistic effect of RA with interferon-β on T suppressor cell augmentation (Qu et al, 1998), others found the association between vitamin A and MRI outcomes to be non-significant during interferon-β use (Loken-Amsrud et al, 2012). We were unable to confirm any of this here.…”

Section: Discussioncontrasting

confidence: 72%

Vitamin A is not associated with exacerbations in multiple sclerosis

Runia

Hop

Rijke

et al. 2014

Multiple Sclerosis and Related Disorders

View full text Add to dashboard Cite

show abstract

Section: Discussioncontrasting

confidence: 72%

Vitamin A is not associated with exacerbations in multiple sclerosis

Runia

Hop

Rijke

et al. 2014

Multiple Sclerosis and Related Disorders

View full text Add to dashboard Cite

show abstract

“…Cyokine receptor antagonists Anti-IL-12/IL-23p40, IL-1RA, lenercept No (worsening with lenercept, no effect with the others (Constantinescu et al, 1998;Chen et al, 2006;Furlan et al, 2007;Martin and Near, 1995) Targeting/depleting immune cells other than T cells Macrophage/microglia depletion Chlodronate No (Huitinga et al, 1990;Jung et al, 1993;Tran et al, 1998) B cell depletion/blockade AntiCD20/CD19 antibodies Yes (promising) (Hauser et al, 2008;Matsushita et al, 2008;Kap et al, 2010b) Yes (small study plus IFN) (Massacesi et al, 1991;Vergelli et al, 1997;Qu et al, 1998) (Sewell et al, 2002Sewell et al, 2003;Correale and Farez, 2009) (Karussis et al, 1992;Burt et al, 1998;van Bekkum, 2000;Burt et al, 2009;Muraro and Uccelli, 2010;Pasquini et al, 2010) Cell trafficking/based approaches Targeting adhesion molecules required...…”

Section: Anti-cytokine Monoclonal Antibodiesmentioning

confidence: 99%

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

Constantinescu

Farooqi

O’Brien

et al. 2011

British J Pharmacology

1,184

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

“…NK cells were enriched with anti-CD3 and anti-CD19 to deplete B cells. (30) B and NK cell purities were .85% based on CD19 or CD56 staining.…”

Section: Isolation Of Mnc and Enrichment For Mnc Subsetsmentioning

confidence: 99%

“…(26) IFNs regulate production of IL-10. In vitro, IFN-b induces small amounts of IL-10 in resting monocytes and mononuclear cells (MNC) (27)(28)(29)(30) and enhances IL-10 secretion is activated T cells. (31,32) In vivo, IFN-b therapy elevates IL-10 mRNA and Department of Neurology, The University of Chicago, Chicago, IL 60637. protein in circulating MNC (29,33,34) and in serum.…”

Section: Introductionmentioning

confidence: 99%

Type I Interferons Inhibit Interleukin-10 Production in Activated Human Monocytes and Stimulate IL-10 in T Cells: Implications for Th1-Mediated Diseases

Feng

Yau

Holbrook

et al. 2002

Journal of Interferon & Cytokine Research

View full text Add to dashboard Cite

Type I interferons (IFNs) directly induce development of Th1 cells. However, IFN-alpha and IFN-beta should generate Th2 cells because these IFNs induce interleukin-10 (IL-10) and block secretion of IFN-gamma. We hypothesized that paradoxical effects of IFNs on Th1-mediated immunity could be from monocyte-specific and T cell-specific IL-10 regulation. We demonstrate that IFN-alpha and IFN-beta inhibit IL-10 mRNA and protein production by activated monocytes but stimulate IL-10 production by activated T cells from the same healthy donors. Without IFN-beta, Staphylococcus aureus, Cowan strain I (SAC)-activated monocytes secreted 15-fold more IL-10 than phorbol myristate acetate (PMA) anti-CD3-activated T cells. With IFN-beta, the two subsets had nearly equivalent secretion. Prostaglandin (PGE) and other cAMP agonists had subset-specific effects on IL-10 production opposite to IFN-beta. The differential IFN-beta effect on transcriptional regulation of IL-10 in monocytes and T cells was from lineage-specific modification of RNA stability. IFN-beta decreased the half-life of IL-10 mRNA in activated monocytes but prolonged the half-life in activated T cells. Subset-specific IL-10 regulation has important implications for Th1-mediated disease. When activated macrophages and microglia are in excess, as in rheumatoid joints or possibly in chronic multiple sclerosis brain lesions, IFNs may inhibit overall IL-10 production and worsen disease. When T cells outnumber monocytes, IFN-beta will induce IL-10 and ameliorate Th1-mediated disease.

show abstract

All-trans Retinoic Acid Potentiates the Ability of Interferon Beta-1b to Augment Suppressor Cell Function in Multiple Sclerosis

Cited by 36 publications

References 42 publications

Vitamin A is not associated with exacerbations in multiple sclerosis

Vitamin A is not associated with exacerbations in multiple sclerosis

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

Type I Interferons Inhibit Interleukin-10 Production in Activated Human Monocytes and Stimulate IL-10 in T Cells: Implications for Th1-Mediated Diseases

Contact Info

Product

Resources

About