Immune surveillance in the central nervous system

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Abstract

Despite being protected by the blood-brain barrier, the CNS must constantly be monitored for insult or pathogen invasion. In this review, the authors illustrate the molecular and cellular players that preside over this surveillance of the brain and spinal cord.

Abstract

The CNS, which consists of the brain and spinal cord, is continuously monitored by resident microglia and blood-borne immune cells such as macrophages, dendritic cells and T cells to detect for damaging agents that would disrupt homeostasis and optimal functioning of these vital organs. Further, the CNS must balance between vigilantly detecting for potentially harmful factors and resolving any immunological responses that in themselves can create damage if left unabated. We discuss the physiological roles of the immune sentinels that patrol the CNS, the molecular markers that underlie their surveillance duties, and the consequences of interrupting their functions following injury and infection by viruses such as JC virus, human immunodeficiency virus, herpes simplex virus and West Nile virus.

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Most cited references 78

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The diseased brain hosts a heterogeneous population of myeloid cells, including parenchymal microglia, perivascular cells, meningeal macrophages and blood-borne monocytes. To date, the different types of brain myeloid cells have been discriminated solely on the basis of their localization, morphology and surface epitope expression. However, recent data suggest that resident microglia may be functionally distinct from bone marrow- or blood-derived phagocytes, which invade the CNS under pathological conditions. During the last few years, research on brain myeloid cells has been markedly changed by the advent of new tools in imaging, genetics and immunology. These methodologies have yielded unexpected results, which challenge the traditional view of brain macrophages. On the basis of these new studies, we differentiate brain myeloid subtypes with regard to their origin, function and fate in the brain and illustrate the divergent features of these cells during neurodegeneration. © 2011 Nature America, Inc. All rights reserved.

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A crucial question in the study of immunological reactions in the central nervous system (CNS) concerns the identity of the parenchymal cells that function as the antigen-presenting cells in that organ. Rat bone marrow chimeras and encephalitogenic, major histocompatability--restricted T-helper lymphocytes were used to show that a subset of endogenous CNS cells, commonly termed "perivascular microglial cells," is bone marrow-derived. In addition, these perivascular cells are fully competent to present antigen to lymphocytes in an appropriately restricted manner. These findings are important for bone marrow transplantation and for neuroimmunological diseases such as multiple sclerosis.

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Microglia, the primary resident immune cells of the central nervous system (CNS), exhibit dynamic behavior involving rapid process motility and cellular migration that is thought to underlie key functions of immune surveillance and tissue repair. Although age-related changes in microglial activation have been implicated in the pathogenesis of neurodegenerative diseases of aging, how dynamic behavior in microglia is influenced by aging is not fully understood. In this study, we employed live imaging of retinal microglia in situ to compare microglial morphology and behavioral dynamics in young and aged animals. We found that aged microglia in the resting state have significantly smaller and less branched dendritic arbors, and also slower process motilities, which probably compromise their ability to survey and interact with their environment continuously. We also found that dynamic microglial responses to injury were age-dependent. While young microglia responded to extracellular ATP, an injury-associated signal, by increasing their motility and becoming more ramified, aged microglia exhibited a contrary response, becoming less dynamic and ramified. In response to laser-induced focal tissue injury, aged microglia demonstrated slower acute responses with lower rates of process motility and cellular migration compared with young microglia. Interestingly, the longer term response of disaggregation from the injury site was retarded in aged microglia, indicating that senescent microglial responses, while slower to initiate, are more sustained. Together, these altered features of microglial behavior at rest and following injury reveal an age-dependent dysregulation of immune response in the CNS that may illuminate microglial contributions to age-related neuroinflammatory degeneration. No claim to original US government works. Aging Cell © 2010 Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland.

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Author and article information

Contributors

Shalina S Ousman: sousman@ucalgary.ca

Paul Kubes: pkubes@ucalgary.ca

Journal

Journal ID (nlm-ta): Nat Neurosci

Journal ID (iso-abbrev): Nat. Neurosci

Title: Nature Neuroscience

Publisher: Nature Publishing Group US (New York )

ISSN (Print): 1097-6256

ISSN (Electronic): 1546-1726

Publication date (Electronic): 26 July 2012

Publication date (Print): 2012

Volume: 15

Issue: 8

Pages: 1096-1101

Affiliations

[1 ]GRID grid.22072.35, ISNI 0000 0004 1936 7697, Department of Clinical Neurosciences, , University of Calgary, ; Calgary, Alberta Canada

[2 ]GRID grid.22072.35, ISNI 0000 0004 1936 7697, Department of Cell Biology & Anatomy, , University of Calgary, ; Calgary, Alberta Canada

[3 ]GRID grid.22072.35, ISNI 0000 0004 1936 7697, Hotchkiss Brain Institute, University of Calgary, ; Calgary, Alberta Canada

[4 ]GRID grid.22072.35, ISNI 0000 0004 1936 7697, Department of Critical Care Medicine, , University of Calgary, ; Calgary, Alberta Canada

[5 ]GRID grid.22072.35, ISNI 0000 0004 1936 7697, Department of Physiology and Pharmacology, , University of Calgary, ; Calgary, Alberta Canada

[6 ]GRID grid.22072.35, ISNI 0000 0004 1936 7697, Snyder Institute of Chronic Diseases, University of Calgary, ; Calgary, Alberta Canada

Article

Publisher ID: BFnn3161

DOI: 10.1038/nn.3161

PMC ID: 7097282

PubMed ID: 22837040

SO-VID: 5301a3a4-31ba-43b0-b153-5fdf2c299123

License:

This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.