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
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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“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]
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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.
- 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
- 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
- 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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