CD163 Identifies a Unique Population of Ramified Microglia in HIV Encephalitis (HIVE)
Abstract
The idea that CNS ramified microglia are quiescent has been challenged by studies that show that microglia without the classic signs of activation can be phagocytic and appear with shorter, thicker ramifications. These semi-activated cells may constitute a form of microglia that has not been previously recognized in neuropathological conditions and may contribute to the pathology and dysfunction in these disorders. This study investigated the expression of CD 163, a cell surface marker whose normal expression is restricted to monocytes/macrophages, in cases of HIV or SIV encephalitis (HIVE/SIVE), Alzheimer disease, and variant Creutzfeldt-Jakob disease. In HIVE/SIVE, in addition to reacting with CNS macrophages, CD163 antibody staining was shown to highlight ramified microglia. Such reactivity was especially notable in grey matter ramified microglia and was greater than that of another typically used marker, HLA-DR. CD163 expression was only observed in infected/affected tissue, in contrast to that shown with another microglia marker, GLUT5, which has recently been shown to identify all microglia regardless of disease state. Although activated microglia were present in the other disorders, as evidenced by strong HLA-DR expression, there was very little CD163 immunoreactivity. The activation state identified by CD163 has not been previously recognized and may have a positive or negative impact on neuronal damage shown in HIV-associated dementia.
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Brain parenchymal CD163 positive macrophages correlate with blood-brain barrier damage in other white matter disorders.
“Brain parenchymal CD163 positive macrophages correlate with blood-brain barrier damage in other white matter disorders [5, 45, 56].”
From Loss of homeostatic microglial phenotype in CSF1R-related Leukoencephalopathy (2020) · cites this paper as [45]
The Results and Discussion (page unavailable) report CD163-positive cells in the brain parenchyma, including white matter, in HIV/SIV encephalitis. They do not report a correlation with blood–brain barrier damage or establish that relationship in other white matter disorders. (LLM, conf=0.82)
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Translating the Brain Transcriptome in NeuroAIDS: From Non-human Primates to Humans
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NeuroAIDS, Drug Abuse, and Inflammation: Building Collaborative Research Activities
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CD8+T Cells Maintain Suppression of Simian Immunodeficiency Virus in the Central Nervous System
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- Authors
- Roberts, E. S., Masliah, E., & Fox, H. S.
- Affiliations
- Scripps Research Institute (US)
- University of California San Diego (US)
- Corresponding author
- Fox, Howard S.
- Venue
- Journal of Neuropathology & Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 2004-12
- Volume
- 63
- Issue
- 12
- Pages
- 1255-1264
- ISSN
- 0022-3069 (ISSN-L)
- 1554-6578
- OpenAlex
- W123631083
- Cited by
- 100
- References
- 52
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 3 · 2023: 2 · 2022: 9 · 2020: 6 · 2018: 8 · 2017: 6 · 2016: 4 · 2015: 4 · 2014: 9 · 2013: 4 · 2012: 10
- FWCI
- 1.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuropathology & Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01mh061224-05)
- National Institute of Mental Health (MH 62261, MH 61224, R01MH061692, MH 61692, R01MH059468, P30MH062261, MH 59468)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- CD163, ramified microglia, HIV encephalitis, SIV encephalitis, microglial activation, HLA-DR, GLUT5, Alzheimer's disease, variant Creutzfeldt-Jakob disease, HIV-associated dementia, phagocytosis
- MeSH terms
- CD163 Antigen, Acquired Immunodeficiency Syndrome, Alzheimer Disease, Animals, Brain, Humans, Immunohistochemistry, Creutzfeldt-Jakob Syndrome, Macaca mulatta, Receptors, Cell Surface, Staining and Labeling, Antigens, Differentiation, Myelomonocytic, AIDS Dementia Complex, Antigens, CD, Case-Control Studies, Simian Acquired Immunodeficiency Syndrome, Microglia, Encephalitis, Viral
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