Anna Zinger1, Sharissa L Latham2, Valery Combes2, Scott Byrne3, Michael H Barnett4, Simon Hawke5, Georges E Grau2. 1. Vascular Immunology Unit, Discipline of Pathology, Sydney Medical School, The University of Sydney, Camperdown, NSW, Australia anna.zinger@sydney.edu.au. 2. Vascular Immunology Unit, Discipline of Pathology, Sydney Medical School, The University of Sydney, Camperdown, NSW, Australia. 3. Cellular Photoimmunology Group, Discipline of Infectious Diseases and Immunology, Sydney Medical School, The Charles Perkins Centre Hub at The University of Sydney, Camperdown, NSW, Australia. 4. Brain and Mind Centre, The University of Sydney, Camperdown, NSW, Australia. 5. Vascular Immunology Unit, Discipline of Pathology, Sydney Medical School, The University of Sydney, Camperdown, NSW, Australia/Brain and Mind Centre, The University of Sydney, Camperdown, NSW, Australia/Central West Neurology & Neurosurgery, Orange, NSW, Australia.
Abstract
BACKGROUND: No molecular marker can monitor disease progression and treatment efficacy in multiple sclerosis (MS). Circulating microparticles represent a potential snapshot of disease activity at the blood brain barrier. OBJECTIVES AND METHODS: To profile plasma microparticles by flow cytometry in MS and determine how fingolimod could impact endothelial microparticles production. RESULTS: In non-treated MS patients compared to healthy and fingolimod-treated patients, endothelial microparticles were higher, while B-cell-microparticle numbers were lower. Fingolimod dramatically reduced tumour necrosis factor (TNF)-induced endothelial microparticle release in vitro. CONCLUSION: Fingolimod restored dysregulated endothelial and B-cell-microparticle numbers, which could serve as a biomarker in MS.
BACKGROUND: No molecular marker can monitor disease progression and treatment efficacy in multiple sclerosis (MS). Circulating microparticles represent a potential snapshot of disease activity at the blood brain barrier. OBJECTIVES AND METHODS: To profile plasma microparticles by flow cytometry in MS and determine how fingolimod could impact endothelial microparticles production. RESULTS: In non-treated MSpatients compared to healthy and fingolimod-treated patients, endothelial microparticles were higher, while B-cell-microparticle numbers were lower. Fingolimod dramatically reduced tumour necrosis factor (TNF)-induced endothelial microparticle release in vitro. CONCLUSION:Fingolimod restored dysregulated endothelial and B-cell-microparticle numbers, which could serve as a biomarker in MS.
Authors: Matías Sáenz-Cuesta; Ainhoa Alberro; Maider Muñoz-Culla; Iñaki Osorio-Querejeta; Marta Fernandez-Mercado; Itziar Lopetegui; Mikel Tainta; Álvaro Prada; Tamara Castillo-Triviño; Juan Manuel Falcón-Pérez; Javier Olascoaga; David Otaegui Journal: Int J Mol Sci Date: 2018-08-19 Impact factor: 5.923
Authors: Felix Marsh-Wakefield; Thomas Ashhurst; Stephanie Trend; Helen M McGuire; Pierre Juillard; Anna Zinger; Anderson P Jones; Allan G Kermode; Simon Hawke; Georges E Grau; Prue H Hart; Scott N Byrne Journal: Clin Transl Immunology Date: 2020-04-29