Neuroimmunity and the blood-brain barrier: molecular regulation of leukocyte transmigration and viral entry into the nervous system with a focus on neuroAIDS
Open accessAbstract
HIV infection of the central nervous system (CNS) can result in neurologic dysfunction with devastating consequences in a significant number of individuals with AIDS. Two main CNS complications in individuals with HIV are encephalitis and dementia, which are characterized by leukocyte infiltration into the CNS, microglia activation, aberrant chemokine expression, blood-brain barrier (BBB) disruption, and eventual damage and/or loss of neurons. One of the major mediators of NeuroAIDS is the transmigration of HIV-infected leukocytes across the BBB into the CNS. This review summarizes new key findings that support a critical role of the BBB in regulating leukocyte transmigration. In addition, we discuss studies on communication among cells of the immune system, BBB, and the CNS parenchyma, and suggest how these interactions contribute to the pathogenesis of NeuroAIDS. We also describe some of the animal models that have been used to study and characterize important mechanisms that have been proposed to be involved in HIV-induced CNS dysfunction. Finally, we review the pharmacologic interventions that address neuroinflammation, and the effect of substance abuse on HIV-1 related neuroimmunity.
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The brain inflammatory response to antigen infiltration triggered by activated microglia may result in aberrant expression of several chemokines, leading to alterations in BBB permeability.
“the brain inflammatory response to antigen infiltration (virus, bacteria or fungus) triggered by activated microglia may result in aberrant expression of several chemokines, leading to alterations in BBB permeability (Buckner et al., 2006; Obermeier et al., 2013).”
From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Buckner et al., 2006
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- Authors
- Buckner, C. M., Luers, A. J., Calderon, T. M., Eugenin, E. A., & Berman, J. W.
- Affiliations
- Albert Einstein College of Medicine (US)
- Corresponding author
- Berman, Joan W.
- Venue
- Journal of Neuroimmune Pharmacology
- Published
- 2006-04-13
- Volume
- 1
- Issue
- 2
- Pages
- 160-181
- ISSN
- 1557-1890 (ISSN-L)
- 1557-1904
- PMC
- PMC4359614
- OpenAlex
- W2018506622
- Cited by
- 88
- References
- 260
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 7 · 2023: 2 · 2022: 2 · 2021: 4 · 2020: 4 · 2019: 5 · 2018: 2 · 2017: 4 · 2016: 2 · 2015: 7 · 2014: 6 · 2013: 2 · 2012: 8
- FWCI
- 3.51
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Neuroimmune Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5r01mh052974-10)
- Center for AIDS Research, University of Washington
- National Institute of Mental Health (K01MH076679, MH0702297, R01MH075679, MH 52974)
- National Institute of Allergy and Infectious Diseases (P30AI051519, AI 051519)
- National Institute of Neurological Disorders and Stroke (T32NS007098, NS-11920, P50NS011920, NS 07098)
- Topics
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- neuroimmunity, blood-brain barrier, HIV infection, neuroAIDS, leukocyte transmigration, HIV-associated encephalitis, HIV-associated dementia, microglial activation, chemokines, neuroinflammation, substance abuse, animal models of HIV, pharmacological interventions
- MeSH terms
- Acquired Immunodeficiency Syndrome, Animals, Blood-Brain Barrier, Brain, Chemotaxis, Leukocyte, Humans, Neuroimmunomodulation, HIV-1, AIDS Dementia Complex, Substance-Related Disorders
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