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4. CXCL13 as a Biomarker: Background and Utility in Multiple Sclerosis.

Author

Pachner, Andrew R., Pike, Steven, Smith, Andrew D., and Gilli, Francesca

Subjects
LYME neuroborreliosis, MULTIPLE sclerosis, MATRIX effect, POINT-of-care testing, BIOMARKERS
Abstract

CXCL13 is a chemokine which is upregulated within the CNS in multiple sclerosis, Lyme neuroborreliosis, and other inflammatory diseases and is increasingly clinically useful as a biomarker. This review provides background for understanding its function in the immune system and its relationship to ectopic lymphoid follicles. Also reviewed are its utility in multiple sclerosis and Lyme neuroborreliosis and potential problems in its measurement. CXCL13 has the potential to be an exceptionally useful biomarker in a range of inflammatory diseases. [ABSTRACT FROM AUTHOR]

Published
2024
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17. Neutralizing Antibodies against IFN-[Beta] in Multiple Sclerosis: Antagonization of IFN-[Beta] Mediated Suppression of MMPs

Author

Gilli, Francesca, Bertolotto, Antonio, and Sala, Arianna

Abstract

Neutralizing antibodies (NAb) against interferon-[Beta] (IFN-Beta) develop in about a third of treated multiple sclerosis patients and are believed to reduce therapeutic efficacy of IFN-[Beta] on clinical and MRI measures. The expression of the interferon acute-response protein, myxovirus resistance protein A (MxA) is a sensitive measure of the biological activity of therapeutically applied IFN-[Beta] and of its reduced bioavailability due to NAb. However, MxA may not be operative in the pathogenesis of multiple sclerosis or the therapeutic effect of IFN-[Beta]. Instead, matrix metalloproteinases (MMPs) are increased in brain tissue, CSF and blood circulation of multiple sclerosis patients and function as effector molecules in several steps of multiple sclerosis pathogenesis. One of the molecular mechanisms by which IFN-[Beta] exerts its beneficial effect in multiple sclerosis is reduction of MMP-9 expression and increase of its endogenous tissue inhibitor, TIMP-1. Quantitative PCR measurements of MMP-2 and MMP-9, TIMP-1 and TIMP-2, and MxA were performed in peripheral mononuclear cells from clinically stable multiple sclerosis patients with relapsing remitting disease course after short-term and long-term treatment with IFN-[Beta]. IFN-[Beta] therapy downregulated the expression of MMP-9 and abolished that of MMP-2 in long-term, but not short-term treated multiple sclerosis, while levels of MxA were increased in both instances. The presence of NAb reversed these effects, i.e. led to reduced MxA and increased MMP-2/MMP-9 expression levels compared with NAb--patients. In contrast, expression of TIMPs in peripheral blood mononuclear cells remained unaffected by IFN-[Beta] therapy and the presence of NAb. While MxA is able to detect the biological action and reduced bioavailability of IFN-[Beta] on the basis of single injections, only MMP-9 shows quantitative correlation with the NAb titre. Together with evidence that an imbalance between MMP and TIMP expression is a crucial pathogenetic feature in multiple sclerosis, these findings support the concept of a significant role of NAb in reducing the therapeutic efficacy of IFN-[Beta]. (Contains 5 figures.)

Published
2004

37. sj-pdf-1-mso-10.1177_2055217320981396 - Supplemental material for Intrathecally produced CXCL13: A predictive biomarker in multiple sclerosis

Author

DiSano, Krista D, Gilli, Francesca, and Pachner, Andrew R

Subjects
FOS: Clinical medicine, 110904 Neurology and Neuromuscular Diseases, Neuroscience
Abstract

Supplemental material, sj-pdf-1-mso-10.1177_2055217320981396 for Intrathecally produced CXCL13: A predictive biomarker in multiple sclerosis by Krista D DiSano, Francesca Gilli and Andrew R Pachner in Multiple Sclerosis Journal – Experimental, Translational and Clinical

Published
2020
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43. Neutralizing antibodies against IFN‐β in multiple sclerosis: antagonization of IFN‐β mediated suppression of MMPs

Author

Gilli, Francesca, Bertolotto, Antonio, Sala, Arianna, Hoffmann, Francine, Capobianco, Marco, Malucchi, Simona, Glass, Tracy, Kappos, Ludwig, Lindberg, Raija L.P., and Leppert, David

Abstract

Neutralizing antibodies (NAb) against interferon‐β (IFN‐β) develop in about a third of treated multiple sclerosis patients and are believed to reduce therapeutic efficacy of IFN‐β on clinical and MRI measures. The expression of the interferon acute‐response protein, myxovirus resistance protein A (MxA) is a sensitive measure of the biological activity of therapeutically applied IFN‐β and of its reduced bioavailability due to NAb. However, MxA may not be operative in the pathogenesis of multiple sclerosis or the therapeutic effect of IFN‐β. Instead, matrix metalloproteinases (MMPs) are increased in brain tissue, CSF and blood circulation of multiple sclerosis patients and function as effector molecules in several steps of multiple sclerosis pathogenesis. One of the molecular mechanisms by which IFN‐β exerts its beneficial effect in multiple sclerosis is reduction of MMP‐9 expression and increase of its endogenous tissue inhibitor, TIMP‐1. Quantitative PCR measurements of MMP‐2 and MMP‐9, TIMP‐1 and TIMP‐2, and MxA were performed in peripheral mononuclear cells from clinically stable multiple sclerosis patients with relapsing remitting disease course after short‐term and long‐term treatment with IFN‐β. IFN‐β therapy down‐regulated the expression of MMP‐9 and abolished that of MMP‐2 in long‐term, but not short‐term treated multiple sclerosis, while levels of MxA were increased in both instances. The presence of NAb reversed these effects, i.e. led to reduced MxA and increased MMP‐2/MMP‐9 expression levels compared with NAb- patients. In contrast, expression of TIMPs in peripheral blood mononuclear cells remained unaffected by IFN‐β therapy and the presence of NAb. While MxA is able to detect the biological action and reduced bioavailability of IFN‐β on the basis of single injections, only MMP‐9 shows quantitative correlation with the NAb titre. Together with evidence that an imbalance between MMP and TIMP expression is a crucial pathogenetic feature in multiple sclerosis, these findings support the concept of a significant role of NAb in reducing the therapeutic efficacy of IFN‐β

Published
2017

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