Conventional DCs sample and present myelin antigens in the healthy CNS and allow parenchymal T cell entry to initiate neuroinflammation
Abstract
In vivo reactivation of myelin-reactive T cells requires conventional DCs but not other brain-resident antigen-presenting cells.
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MHC-II expression on CNS-resident microglia/macrophages is dispensable for T cell priming and EAE pathogenesis.
“Recently however, a series of studies utilizing different transgenic approaches elegantly showed that MHC-II expression on CNS-resident microglia/macrophages is dispensable for T cell priming and EAE pathogenesis [125, 174, 236, 351].”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [236]
In vitro studies demonstrated that moDC are less capable of presenting myelin compared to cDC, and are therefore redundant in activating autoreactive T cells.
“However, the critical antigen-presenting role of moDC in EAE pathogenesis has been challenged by in vitro studies demonstrating that moDC are less capable of presenting myelin compared to cDC, and are therefore redundant in activating autoreactive T cells [125, 236].”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [236]
CNS-infiltrating myeloid cells showed prolonged interactions with T cells in the CNS and their expression of MHC-II was essential for EAE development.
“It was recently demonstrated that, in contrast to the resident population, CNS-infiltrating myeloid cells showed prolonged interactions with T cells in the CNS and that their expression of MHC-II was essential for EAE development [174, 236].”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [236]
The aforementioned studies implicated cDC2 type of APC in the initiation of EAE.
“Instead, although this topic remains debated, the aforementioned studies implicated cDC2 type of APC in the initiation of EAE.”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [236]
Definitive evidence of a non-redundant role for monocyte-derived APC in activating autoreactive T cells is lacking.
“As both peripherally-derived and CNS-resident myeloid cells have been implicated in antigen presentation to autoreactive T cells, definitive evidence of a non-redundant role for monocyte-derived APC in activating autoreactive T cells is lacking.”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [236]
Immune surveillance and the initiation of CNS immune responses is dependent on antigen-presenting cells that reside alongside important barriers such as perivascular spaces, leptomeningeal vessels, the choroid plexus, and the subarachnoid space.
“Immune surveillance and the initiation of CNS immune responses is dependent on antigen-presenting cells (APCs) that reside alongside important barriers such as perivascular spaces, leptomeningeal vessels, the choroid plexus, and the subarachnoid space (65-68).”
From The anatomy and immunology of vasculature in the central nervous system (2019) · cites this paper as [67]
Upon extravasation, autoreactive T cells interact with peptide-MHC II-bearing APCs in perivascular spaces, triggering up-regulation of chemokines that recruit myeloid cells and release of TNFα that increases production of MMP-2 and MMP-9 by resident and recruited myeloid cells.
“Upon extravasation, the autoreactive T cells interact with peptide–major histocompatibility complex (MHC) II–bearing APCs (such as DCs) in the perivascular spaces, triggering up-regulation of chemokines that recruit myeloid cells and release of TNFα that increases production of metalloproteinases MMP-2 and MMP-9 by resident and recruited myeloid cells (Fig. 4) (65, 67, 84, 119, 120).”
From The anatomy and immunology of vasculature in the central nervous system (2019) · cites this paper as [67]
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“Recently however, a series of studies utilizing different transgenic approaches elegantly showed that MHC-II expression on CNS-resident microglia/macrophages is dispensable for T cell priming and EAE pathogenesis [125, 174, 236, 351].”
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- Authors
- Mundt, S., Mrdjen, D., Utz, S. G., Greter, M., Schreiner, B., & Becher, B.
- Affiliations
- University of Zurich (CH)
- Corresponding author
- Mrdjen, Dunja
- Utz, Sebastian G.
- Becher, Burkhard
- Venue
- Science Immunology
- Published
- 2019-01-04
- Volume
- 4
- Issue
- 31
- ISSN
- 2470-9468 (ISSN-L)
- OpenAlex
- W2913625932
- Cited by
- 235
- References
- 56
- Citations by year
- 2026: 14 · 2025: 27 · 2024: 27 · 2023: 30 · 2022: 38 · 2021: 45 · 2020: 30 · 2019: 23 · 2018: 1
- FWCI
- 14.98
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science Immunology (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Funders
- Swiss National Science Foundation (310030_146130, 316030_150768, 310030_170320)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- myeloid dendritic cells, neuroinflammation, T cell licensing, central nervous system, border-associated macrophages, microglia, autoimmunity
- MeSH terms
- Animals, Antigens, Histocompatibility Antigens Class II, Central Nervous System, Dendritic Cells, Encephalomyelitis, Autoimmune, Experimental, Female, Male, Mice, Inbred C57BL, Mice, Transgenic, Myelin Sheath, T-Lymphocytes, Microglia, Antigen Presentation, Adoptive Transfer
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