Glatiramer acetate-reactive peripheral blood mononuclear cells respond to multiple myelin antigens with a Th2-biased phenotype

Dhib‐Jalbut, Suhayl; Chen, Man; Said, Areen; Zhan, Min; Johnson, Kenneth P.; Martin, Roland

doi:10.1016/s0165-5728(03)00170-x

Cited by 45 publications

(23 citation statements)

References 37 publications

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“…No laquinimod treatmentspecific changes were observed at any time after commencement of study, in any of the factors measured. Our choice to assess changes in the proliferative response and the cytokine/chemokine bias was based on published observations showing changes in the response of PBMC from patients treated with conventional MS therapies including glatiramer acetate and interferons (Brod et al, 1996;Miller et al, 1998;Weber et al, 1999;Duda et al, 2000;Neuhaus et al, 2002;Dhib-Jalbut et al, 2003;Dhib-Jalbut and Marks, 2010;Racke et al, 2010). However, based on more recent observations showing that laquinimod treatment in mice correlated with the development of both anti-inflammatory type II monocytes (SchulzeTopphoff et al, 2012;Thone et al, 2012) and DC (Schulze-Topphoff et al, 2012) we may have been better served assessing the effects of laquinimod on myeloid subpopulations and the innate immune system in general.…”

Section: Discussionmentioning

confidence: 99%

Assessment of changes in immune measures of multiple sclerosis patients treated with laquinimod

Lund

Kelland

Hayardeny

et al. 2013

Journal of Neuroimmunology

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Section: Discussionmentioning

confidence: 99%

Assessment of changes in immune measures of multiple sclerosis patients treated with laquinimod

Lund

Kelland

Hayardeny

et al. 2013

Journal of Neuroimmunology

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“…In this context, IFN-β can enhance TGF-β and IL-10 production from DCs and also suppress IL-23, resulting in reduced differentiation of naïve Th0 cells toward Th17 cells (BartosikPsujek et al 2010;Ramgolam and Markovic-Plese 2010;Zhang and Markovic-Plese 2010). In addition, glatiramer acetate is able to reduce IL-12 production in mDCs (Ruggieri et al 2008), thus promoting Th2 and Treg differentiation (Dhib-Jalbut et al 2003;Weber et al 2007). It is clear, therefore, that DCs are involved in relapse or exacerbation of MS.…”

Section: Dendritic Cellsmentioning

confidence: 99%

The Molecular Mechanisms of Vitamin A Deficiency in Multiple Sclerosis

et al. 2016

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Vitamin A, considered to be an essential nutrient, has important actions in immunological responses and the central nervous system (CNS). Neuroimmunological functions of vitamin A are mediated through its active metabolite, retinoic acid (RA). In the CNS, RA contributes to regeneration and plasticity, while also playing a key role in enhancing tolerance and reducing inflammatory responses by regulating T cell, B cell and dendritic cell populations. However, evidence has indicated lower plasma levels of vitamin A in patients with multiple sclerosis (MS). Vitamin A deficiency leads to dysregulation of immune tolerance and pathogenic immune cell production in this disease. Vitamin A may ameliorate MS pathogenesis through numerous mechanisms including a reduction in inflammatory processes by re-establishing the balance between pathogenic (Th1, Th17, Th9) and immunoprotective cells (Th2, Tregs), modulating B cell and dendritic cell function as well as increasing tolerance of autoimmunity and regeneration in the CNS. Thus, the results from the current review suggest that vitamin A can be considered as a potential treatment in MS disease management.

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“…Originally developed to induce EAE, it was found to actually efficiently suppress the disease when in aqueous form [99,100] The mechanism of action of GA appears to involve the induction of GA--reactive regulatory T cells [30,31] and/or inhibition of APCs such as dendritic cells (DCs) and monocytes [109]. In primates, GA was used to treat on-going disease [87].…”

Section: Copaxone ®mentioning

confidence: 99%

Treating autoimmune diseases through restoration of antigen-specific immune tolerance

Wolfraim

2006

Arch. Immunol. Ther. Exp.

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The first line of treatment for many human autoimmune diseases involves the use of anti-inflammatory or immunosuppressive drugs such as prednisone or other steroids that not only suppress the underlying autoimmune disease, but lead to global suppression of the immune system. The sequelae of this approach include increased risk of infection, carcinogenesis, and osteoporosis. Moreover, such broad spectrum immunosuppression tends to have transient therapeutic benefit, as in many cases the disease becomes refractory to these drugs. There is a clear need for more specific means to restore immune tolerance to the specific autoantigens implicated in disease pathology. This review provides an overview of some of these newer, more specific therapeutic approaches to restoring immune tolerance to autoantigens, with an emphasis on those approaches that have been or will soon be tested in controlled clinical trials. Covered here are peptide- or protein-based therapeutics, oral tolerance, and cellular and gene therapy approaches to restoring antigen-specific immune tolerance.

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Glatiramer acetate-reactive peripheral blood mononuclear cells respond to multiple myelin antigens with a Th2-biased phenotype

Cited by 45 publications

References 37 publications

Assessment of changes in immune measures of multiple sclerosis patients treated with laquinimod

Assessment of changes in immune measures of multiple sclerosis patients treated with laquinimod

The Molecular Mechanisms of Vitamin A Deficiency in Multiple Sclerosis

Treating autoimmune diseases through restoration of antigen-specific immune tolerance

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