The immunology of multiple sclerosis

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The immunology of multiple sclerosis. / Attfield, Kathrine E; Jensen, Lise Torp; Kaufmann, Max; Friese, Manuel A; Fugger, Lars.

in: NAT REV IMMUNOL, Jahrgang 22, Nr. 12, 12.2022, S. 734–750.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ReviewForschung

Harvard

Attfield, KE, Jensen, LT, Kaufmann, M, Friese, MA & Fugger, L 2022, 'The immunology of multiple sclerosis', NAT REV IMMUNOL, Jg. 22, Nr. 12, S. 734–750. https://doi.org/10.1038/s41577-022-00718-z

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Bibtex

@article{9b20b9cb8f1f49eb9610ff522b02ab41,
title = "The immunology of multiple sclerosis",
abstract = "Our incomplete understanding of the causes and pathways involved in the onset and progression of multiple sclerosis (MS) limits our ability to effectively treat this complex neurological disease. Recent studies explore the role of immune cells at different stages of MS and how they interact with cells of the central nervous system (CNS). The findings presented here begin to question the exclusivity of an antigen-specific cause and highlight how seemingly distinct immune cell types can share common functions that drive disease. Innovative techniques further expose new disease-associated immune cell populations and reinforce how environmental context is critical to their phenotype and subsequent role in disease. Importantly, the differentiation of immune cells into a pathogenic state is potentially reversible through therapeutic manipulation. As such, understanding the mechanisms that provide plasticity to causal cell types is likely key to uncoupling these disease processes and may identify novel therapeutic targets that replace the need for cell ablation.",
author = "Attfield, {Kathrine E} and Jensen, {Lise Torp} and Max Kaufmann and Friese, {Manuel A} and Lars Fugger",
note = "{\textcopyright} 2022. Springer Nature Limited.",
year = "2022",
month = dec,
doi = "10.1038/s41577-022-00718-z",
language = "English",
volume = "22",
pages = "734–750",
journal = "NAT REV IMMUNOL",
issn = "1474-1733",
publisher = "NATURE PUBLISHING GROUP",
number = "12",

}

RIS

TY - JOUR

T1 - The immunology of multiple sclerosis

AU - Attfield, Kathrine E

AU - Jensen, Lise Torp

AU - Kaufmann, Max

AU - Friese, Manuel A

AU - Fugger, Lars

N1 - © 2022. Springer Nature Limited.

PY - 2022/12

Y1 - 2022/12

N2 - Our incomplete understanding of the causes and pathways involved in the onset and progression of multiple sclerosis (MS) limits our ability to effectively treat this complex neurological disease. Recent studies explore the role of immune cells at different stages of MS and how they interact with cells of the central nervous system (CNS). The findings presented here begin to question the exclusivity of an antigen-specific cause and highlight how seemingly distinct immune cell types can share common functions that drive disease. Innovative techniques further expose new disease-associated immune cell populations and reinforce how environmental context is critical to their phenotype and subsequent role in disease. Importantly, the differentiation of immune cells into a pathogenic state is potentially reversible through therapeutic manipulation. As such, understanding the mechanisms that provide plasticity to causal cell types is likely key to uncoupling these disease processes and may identify novel therapeutic targets that replace the need for cell ablation.

AB - Our incomplete understanding of the causes and pathways involved in the onset and progression of multiple sclerosis (MS) limits our ability to effectively treat this complex neurological disease. Recent studies explore the role of immune cells at different stages of MS and how they interact with cells of the central nervous system (CNS). The findings presented here begin to question the exclusivity of an antigen-specific cause and highlight how seemingly distinct immune cell types can share common functions that drive disease. Innovative techniques further expose new disease-associated immune cell populations and reinforce how environmental context is critical to their phenotype and subsequent role in disease. Importantly, the differentiation of immune cells into a pathogenic state is potentially reversible through therapeutic manipulation. As such, understanding the mechanisms that provide plasticity to causal cell types is likely key to uncoupling these disease processes and may identify novel therapeutic targets that replace the need for cell ablation.

U2 - 10.1038/s41577-022-00718-z

DO - 10.1038/s41577-022-00718-z

M3 - SCORING: Review article

C2 - 35508809

VL - 22

SP - 734

EP - 750

JO - NAT REV IMMUNOL

JF - NAT REV IMMUNOL

SN - 1474-1733

IS - 12

ER -