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Biomedical subjects

Yanina Galboiz

Publications and source records attributed to Yanina Galboiz.

6 recordsLinked to original sources

Vitamin B12, demyelination, remyelination and repair in multiple sclerosis.

Multiple Sclerosis (MS) and vitamin B12 deficiency share common inflammatory and neurodegenerative pathophysiological characteristics. Due to similarities in the clinical presentations and MRI findings, the differential diagnosis between vitamin B12 deficiency and MS may be difficult. Additionally, low or decreased levels of vitamin B12 have been demonstrated in MS patients. Moreover, recent studies suggest that vitamin B12, in addition to its known role as a co-factor in myelin formation, has important immunomodulatory and neurotrophic effects. These observations raise the questions of possible causal relationship between the two disorders, and suggest further studies of the need to close monitoring of vitamin B12 levels as well as the potential requirement for supplementation of vitamin B12 alone or in combination with the immunotherapies for MS patients.

Animals↗

The 'immunological-synapse' at its APC side in relapsing and secondary-progressive multiple sclerosis: modulation by interferon-beta.

Reciprocal interactions between T cells and antigen-presenting cells (APCs) within the 'Immunological-Synapse' (IS) govern immune cell autoreactivity in multiple sclerosis (MS). The present study examined the expression of a range of co-stimulatory molecules: CD40, CD54, CD80, CD86 and HLA-DR, on the cell-surface of CD14(+) peripheral blood monocytes (PBM) from relapsing-remitting (RR) and secondary-progressive (SP)-MS patients, prior to and during 1 year of Interferon (IFN)-beta-1a (Rebif(R)) therapy. Prior to treatment, patients from both MS subtypes expressed elevated CD80 and reduced CD40 levels in comparison to controls. CD86 expression was significantly reduced in SP compared to RR patients and controls. IFN-beta therapy led to a significant reduction in the expression of CD54 and CD80 in both groups of patients as well as to elevation of CD40 and CD86 expression in SP patients. These results confirm IFN-mediated modulation of the APC surface within the immunological-synapse and implicate CD80 and CD86 as targets for interventional therapies in MS as well as other Th1-mediated autoimmune diseases.

Adjuvants, Immunologic↗

Modulation of monocytes matrix metalloproteinase-2, MT1-MMP and TIMP-2 by interferon-gamma and -beta: implications to multiple sclerosis.

Recent findings have implicated the activity of matrix metalloproteinases (MMPs) in the pathogenesis of multiple sclerosis (MS), while in vivo interferon (IFN)-beta treatment was demonstrated to suppress MMPs. In the present study, the effects mediated by IFN-gamma and IFN-beta on the mRNA and protein expression of MMP-2, its physiological activator, MT1-MMP and its endogenous inhibitor, TIMP-2, by monocytes were evaluated in vitro. The results point to the significance of IFNs in modulating MMPs/tissue inhibitors of MMPs (TIMPs) expression, and support the possibility that the therapeutic effects of IFN-beta may be, in part, due to induction of a shift from "pro-" to "anti-proteolytic" pattern of MMPs and TIMPs expression.

Dose-Response Relationship, Drug↗

Immunological indicators of disease activity and prognosis in multiple sclerosis.

The need to ensure an accurate diagnosis and proper treatment for multiple sclerosis patients, considering the various clinical and immunopathological subtypes of the disease, requires the identification of biomarkers that measure disease activity and predict the course of disease development in individual patients. Moreover, the identification of effective indicators will lead not only to optimized patient treatment but also to the development of better tools for evaluating clinical trials. Recent studies focusing on the identification of possible immunological markers in multiple sclerosis will be reviewed.

Antigens, Surface↗