ArticlePloS one2012
Excess soluble CD40L contributes to blood brain barrier permeability in vivo: implications for HIV-associated neurocognitive disorders.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 66 citations in OpenAlex.
- Characterization of platelet-monocyte complexes in HIV-1-infected individuals: possible role in HIV-associated neuroinflammation.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
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- P-Selectin and Platelet-Monocyte Interaction in Inflammation: Mechanisms, Hypothesis, and Open Questions.Journal of inflammation research · 2026Review
- Dengue infection changes the expressions of CD154 and CD148 in human platelets.Virus research · 2025Article
- Schizophrenia endothelial cells exhibit higher permeability and altered angiogenesis patterns in patient-derived organoids.Translational psychiatry · 2024Article
- Systemic inflammatory markers of persistent cerebral edema after aneurysmal subarachnoid hemorrhage.Journal of neuroinflammation · 2022Article
- Emerging therapies to target CNS pathophysiology in multiple sclerosis.Nature reviews. Neurology · 2022Review
- Platelet-Released Factors: Their Role in Viral Disease and Applications for Extracellular Vesicle (EV) Therapy.International journal of molecular sciences · 2022Review
- Circulating brain-derived extracellular vesicles expressing neuroinflammatory markers are associated with HIV-related neurocognitive impairment.Frontiers in immunology · 2022Article
- Obstructive Sleep Apnea, Hypercoagulability, and the Blood-Brain Barrier.Journal of clinical medicine · 2021Review
- Monocytes complexed to platelets differentiate into functionally deficient dendritic cells.Journal of leukocyte biology · 2021Article
- Platelet-endothelial associations may promote cytomegalovirus replication in the salivary gland in mice.Platelets · 2020Article
- Novel Mechanism of Microvesicle Regulation by the Antiviral Protein Tetherin During HIV Infection.Journal of the American Heart Association · 2020Article
- Article
- Platelets Endocytose Viral Particles and Are Activated via TLR (Toll-Like Receptor) Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Dynamics of Transforming Growth Factor (TGF)-β Superfamily Cytokine Induction During HIV-1 Infection Are Distinct From Other Innate Cytokines.Frontiers in immunology · 2020Article
- Hyperglycemia-Driven Neuroinflammation Compromises BBB Leading to Memory Loss in Both Diabetes Mellitus (DM) Type 1 and Type 2 Mouse Models.Molecular neurobiology · 2019Article
- Exposure to traffic-generated air pollutants mediates alterations in brain microvascular integrity in wildtype mice on a high-fat diet.Environmental research · 2018Article
- A Perspective of Coagulation Dysfunction in Multiple Sclerosis and in Experimental Allergic Encephalomyelitis.Frontiers in neurology · 2018Review
- Platelets in Immune Response to Virus and Immunopathology of Viral Infections.Frontiers in medicine · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Despite the use of anti-retroviral therapies, a majority of HIV-infected individuals still develop HIV-Associated Neurocognitive Disorders (HAND), indicating that host inflammatory mediators, in addition to viral proteins, may be contributing to these disorders. Consistently, we have previously shown that levels of the inflammatory mediator soluble CD40L (sCD40L) are elevated in the circulation of HIV-infected, cognitively impaired individuals as compared to their infected, non-impaired counterparts. Recent studies from our group suggest a role for the CD40/CD40L dyad in blood brain barrier (BBB) permeability and interestingly, sCD40L is thought to regulate BBB permeability in other inflammatory disorders of the CNS. Using complementary multiphoton microscopy and quantitative analyses in wild-type and CD40L deficient mice, we now reveal that the HIV transactivator of transcription (Tat) can induce BBB permeability in a CD40L-dependent manner. This permeability of the BBB was found to be the result of aberrant platelet activation induced by Tat, since depletion of platelets prior to treatment reversed Tat-induced BBB permeability. Furthermore, Tat treatment led to an increase in granulocyte antigen 1 (Gr1) positive monocytes, indicating an expansion of the inflammatory subset of cells in these mice, which were found to adhere more readily to the brain microvasculature in Tat treated animals. Exploring the mechanisms by which the BBB becomes compromised during HIV infection has the potential to reveal novel therapeutic targets, thereby aiding in the development of adjunct therapies for the management of HAND, which are currently lacking.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.