Title (en)
Innate Lymphoid Cells - Neglected Players in Multiple Sclerosis
Language
English
Description (en)
Multiple sclerosis (MS) is a highly debilitating autoimmune disease affecting millions of individuals worldwide. Although classically viewed as T-cell mediated disease, the role of innate lymphoid cells (ILC) such as natural killer (NK) cells and ILC 1-3s has become a focal point as several findings implicate them in the disease pathology. The role of ILCs in MS is still not completely understood as controversial findings have been reported assigning them either a protective or disease-accelerating role. Recent findings in experimental autoimmune encephalomyelitis (EAE) suggest that ILCs infiltrate the central nervous system (CNS), mediate inflammation, and have a disease exacerbating role by influencing the recruitment of autoreactive T-cells. Elucidating the detailed role of ILCs and altered signaling pathways in MS is essential for a more complete picture of the disease pathology and novel therapeutic targets. We here review the current knowledge about ILCs in the development and progression of MS and preclinical models of MS and discuss their potential for therapeutic applications.
Keywords (en)
Experimental Autoimmune Encephalomyelitis; Natural-Killer-Cells; Central-Nervous-System; Nk-Cells; Peripheral-Blood; Interferon-Beta; Mechanisms; Biology; Demyelination; Natalizumab
DOI
10.3389/fimmu.2022.909275
Author of the digital object
Negar Sadeghi Hassanabadi (University of Veterinary Medicine Vienna)
Dagmar Gotthardt (University of Veterinary Medicine Vienna)
Bieke Broux (Hasselt University)
Sonja Marinović (Ruder Boskovic Institute)
Format
application/pdf
Size
4.0 MB
Licence Selected
Type of publication
Article
Name of Publication (en)
Frontiers in Immunology
Pages or Volume
10
Volume
13
Publisher
Frontiers Media Sa
Publication Date
2022
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Persistent identifier
DOI
https://phaidra.vetmeduni.ac.at/o:1993
https://doi.org/10.3389/fimmu.2022.909275 - Content
- DetailsObject typePDFDocumentFormatapplication/pdfCreated17.08.2023 07:59:40 UTC
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