Contribution of Dysregulated B-Cells and IgE Antibody Responses to Multiple Sclerosis

Multiple sclerosis (MS), a debilitating autoimmune inflammatory disease that affects the brain and spinal cord, causes demyelination of neurons, axonal damage, and neurodegeneration. MS and the murine experimental autoimmune encephalomyelitis (EAE) model have been viewed mainly as T-cell-mediated di...

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Published inFrontiers in immunology Vol. 13; p. 900117
Main Authors Seals, Malik R., Moran, Monica M., Leavenworth, Jonathan D., Leavenworth, Jianmei W.
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 16.06.2022
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Summary:Multiple sclerosis (MS), a debilitating autoimmune inflammatory disease that affects the brain and spinal cord, causes demyelination of neurons, axonal damage, and neurodegeneration. MS and the murine experimental autoimmune encephalomyelitis (EAE) model have been viewed mainly as T-cell-mediated diseases. Emerging data have suggested the contribution of B-cells and autoantibodies to the disease progression. However, the underlying mechanisms by which dysregulated B-cells and antibody response promote MS and EAE remain largely unclear. Here, we provide an updated review of this specific subject by including B-cell biology and the role of B-cells in triggering autoimmune neuroinflammation with a focus on the regulation of antibody-producing B-cells. We will then discuss the role of a specific type of antibody, IgE, as it relates to the potential regulation of microglia and macrophage activation, autoimmunity and MS/EAE development. This knowledge can be utilized to develop new and effective therapeutic approaches to MS, which fits the scope of the Research Topic “Immune Mechanism in White Matter Lesions: Clinical and Pathophysiological Implications”.
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This article was submitted to Multiple Sclerosis and Neuroimmunology, a section of the journal Frontiers in Immunology
Edited by: Long-Jun Wu, Mayo Clinic, United States
Reviewed by: Judith Fraussen, University of Hasselt, Belgium; Tingjun Chen, Mayo Clinic, United States
These authors have contributed equally to this work
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2022.900117