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

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
Open this paper in CoChat — free account

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.

Integrity signals

Registry

Crossref · 10.1196/annals.1394.023

Cites

59 of 59 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Elucidation of the temporal dynamics of immune cell recruitment in the brains of mice with EAE provides a valuable tool for studying the contribution of leukocyte trafficking to cytokine signalling and sickness/depression-like behaviour.

    “Elucidation of the temporal dynamics of immune cell recruitment in the brains of mice with EAE90,91 provides a valuable tool for studying the contribution of leukocyte trafficking to the activation of cytokine signalling in the brain and to the development of sickness and depression-like behaviour in this model.”

    From From inflammation to sickness and depression: when the immune system subjugates the brain (2008) · cites this paper as [91]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

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 › Pathology and Forensic Medicine › 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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review