The role of peripheral immune cells in the CNS in steady state and disease
Abstract
The CNS is protected by the immune system, including cells that reside directly within the CNS and help to ensure proper neural function, as well as cells that traffic into the CNS with disease. The CNS-resident immune system is comprised mainly of innate immune cells and operates under homeostatic conditions. These myeloid cells in the CNS parenchyma and at CNS-periphery interfaces are highly specialized but also extremely plastic cells that immediately react to any changes in CNS homeostasis and become reactive in the context of neurodegenerative disorders such as Alzheimer's disease or Parkinson's disease. However, when the blood-brain barrier is impaired during CNS diseases such as multiple sclerosis or altered with cerebral ischemia, peripheral adaptive and innate immune cells, including monocytes, neutrophils, T cells and B cells, can enter the CNS, where they execute distinct cell-mediated effects. On the basis of these observations, we assess strategies for targeting peripheral immune cells to reduce CNS disease burden.
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Systemic inflammation, infection, autoimmune disease, injuries, and neurodegenerative diseases often increase the BBB permeability, allowing inflammatory mediators such as cytokines and chemokines, peripheral leukocytes such as monocytes, macrophages, and CD4+ T cells to enter the parenchyma and accelerate disease progression.
“Systemic inflammation, infection, autoimmune disease, injuries, and neurodegenerative diseases often increase the BBB permeability, allowing inflammatory mediators such as cytokines and chemokines, peripheral leukocytes such as monocytes, macrophages, and CD4 + T cells to enter the parenchyma and accelerate disease progression (484).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [484]
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- Authors
- Prinz, M., & Priller, J.
- Affiliations
- University of Freiburg (DE)
- German Center for Neurodegenerative Diseases (DE)
- Corresponding author
- Prinz, Marco
- Priller, Josef
- Venue
- Nature Neuroscience
- Published
- 2017-01-16
- Volume
- 20
- Issue
- 2
- Pages
- 136-144
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- OpenAlex
- W2577452028
- Cited by
- 657
- References
- 38
- Citations by year
- 2026: 42 · 2025: 79 · 2024: 85 · 2023: 77 · 2022: 65 · 2021: 90 · 2020: 57 · 2019: 65 · 2018: 62 · 2017: 34
- FWCI
- 5.73
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- DZNE Pub (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Medical Research Council (MC_PC_16031)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Keywords
- peripheral immune cells, central nervous system, neuroinflammation, blood-brain barrier, myeloid cells, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease, multiple sclerosis, cerebral ischemia, monocytes, neutrophils, T cells, B cells, innate immunity, adaptive immunity, immune cell trafficking, CNS homeostasis
- MeSH terms
- Animals, Blood-Brain Barrier, Central Nervous System, Central Nervous System Diseases, Humans, Monocytes, Neutrophils, T-Lymphocytes
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