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About the Authors:
Simone C. Wuest
Affiliation: Neuroimmunological Diseases Unit, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America
Ina Mexhitaj
Affiliation: Neuroimmunological Diseases Unit, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America
Noo Ri Chai
Affiliation: Neuroimmunological Diseases Unit, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America
Elena Romm
Affiliation: Neuroimmunological Diseases Unit, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America
Joerg Scheffel
Affiliation: Molecular Immunology Section, Laboratory of Molecular Immunogenetics, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, United States of America
Biying Xu
Affiliation: Imaging Probe Development Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, United States of America
Kelly Lane
Affiliation: Imaging Probe Development Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, United States of America
Tianxia Wu
Affiliation: Clinical Neurosciences Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America
Bibiana Bielekova
* E-mail: [email protected]
Affiliation: Neuroimmunological Diseases Unit, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America
Introduction
Multiple sclerosis (MS), the most prevalent neuroimmunological disorder in young adults, is primarily characterized by demyelination and axonal loss and leads to severe disability over time [1]. Analogous to experimental autoimmune encephalomyelitis (EAE), which can be induced in genetically susceptible animals through immunization with varied myelin epitopes, MS has been considered to be mediated by CD4+ Th1/Th17 cells that specifically target myelin. Yet, despite significant efforts to verify myelin target(s), to identify new antigens (Ag's) or to define pathogenic immune cell types, we have to conclude that mechanisms by which the immune system mediates tissue destruction of the central nervous system (CNS) in MS remain unclear.
The majority of published studies addressing Ag-specificity of T cells in MS derived both T cells and Ag-presenting cells (APCs) from peripheral blood mononuclear cells (PBMCs) [2]–[4]. Due to the limited number of professional APCs in...