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Cited by 144Multiple Sclerosis Research StudiesImmunotherapy and Immune ResponsesT-cell and B-cell Immunology

The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.

Antigen Presentation in the CNS by Myeloid Dendritic Cells Drives Progression of Relapsing Experimental Autoimmune Encephalomyelitis

MILLER, STEPHEN D., McMAHON, EILEEN J., SCHREINER, BETTINA, BAILEY, SAMANTHA L.·2007·Annals of the New York Academy of Sciences
DOI 10.1196/annals.1394.023
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Abstract

Abstract: Chronic progression of relapsing experimental autoimmune encephalomyelitis (R‐EAE), a mouse model of multiple sclerosis (MS), is dependent on the activation of T cells to endogenous myelin epitopes, that is, epitope spreading. This review focuses on the cellular and molecular mechanisms underlying the process of epitope spreading. Surprisingly, activation of naïve T cells to endogenous myelin epitopes in SJL mice undergoing R‐EAE occurs directly in the central nervous system (CNS), a site generally perceived to be immunologically privileged. Determination of the antigen presentation capacity of antigen‐presenting cell (APC) populations purified from the CNS of mice with established R‐EAE shows that peripherally derived CD11b+CD11c+CD45 hi myeloid dendritic cells (mDCs) most efficiently present endogenous myelin antigens to activate both preactivated effector myelin‐specific T cells and naïve T cells. The mDCs, which drive epitope spreading, preferentially polarize pathogenic Th17 responses correlating with their enhanced expression of TGF‐β1, IL‐6, and IL‐23. Both B220+CD11c+ plasmacytoid (pDCs) and CD8α+CD11c+ (CD8 DCs) were superior to CD11b+CD11c–CD45 hi macrophages, but less efficient than mDCs at presenting endogenous peptide to induce Th17 cells. In contrast, CNS‐resident CD11b+CD11c–CD45 low microglia purified from the inflamed CNS were found to be largely incapable of activating either naïve or effector T cells.

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Crossref · 10.1196/annals.1394.023

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Metadata

Authors
MILLER, S. D., McMAHON, E. J., SCHREINER, B., & BAILEY, S. L.
Affiliations
  • Northwestern University (US)
  • Westmont College (US)
Corresponding author
MILLER, STEPHEN D.
ORCID
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2007-04
Volume
1103
Issue
1
Pages
179-191
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
DOI
10.1196/annals.1394.023
OpenAlex
W2099046115
Cited by
144
References
59
Citations by year
2026: 1 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 5 · 2021: 8 · 2020: 1 · 2019: 1 · 2018: 9 · 2017: 8 · 2016: 7 · 2015: 14 · 2014: 7 · 2013: 7 · 2012: 16
FWCI
10.37
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 40 d)
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
multiple sclerosis, antigen presentation, myeloid dendritic cells, epitope spreading, Th17 polarization, plasmacytoid dendritic cells, CD8α+ dendritic cells, microglia, macrophages, T cell activation, TGF-β1, IL-23, interleukin-6, SJL mice
MeSH terms
Animals, Epitopes, Central Nervous System, Chronic Disease, Dendritic Cells, Disease Models, Animal, Encephalomyelitis, Autoimmune, Experimental, Mice, Inbred Strains, Multiple Sclerosis, Recurrence, Models, Immunological, Disease Progression, Mice

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