Peter J. Gaskill

This study shows human macrophages have functional CYP3A4 activity, with expression and function discordance, and cocaine increases CYP3A4 activity across donors.

This study shows dopamine modulates macrophage inflammation through epigenetic changes, including DNA methylation and histone modifications, and highlights individual variability in response.

This study shows CBD reduces viral replication and immune activation in HIV/SIV models, suggesting it could be a useful adjunct to antiretroviral therapy.

This paper identifies a pathway where dopamine induces mitochondrial dysfunction in macrophages, leading to IL-6 secretion via the cGAS-STING pathway.

This study shows that neuroinflammatory interactions between microglia and astrocytes in an iPSC model enhance HIV replication through TNF and NF-kB pathways.

This paper identifies that lipid nanoparticle-induced inflammation arises from endosomal membrane damage and proposes strategies to mitigate it through galectin inhibition or ESCRT-recruiting lipids.

This study shows cocaine enhances HIV infection of microglia via sigma-1 activation, which modulates the UPR to boost viral replication and immune evasion.

This paper introduces a high-content imaging assay to quantify HIV-1 infectivity using modified osteosarcoma cells, enabling rapid and consistent evaluation of viral replication dynamics.

This paper analyzes melanoma in people living with HIV, finding impaired antitumor immunity, delayed ICI treatment, and an immunosuppressive tumor microenvironment.

This study shows dopamine increases IL-1β in myeloid cells via differential dopamine receptor expression, and this effect is exacerbated by HIV.

This study shows HIV-infected mice show impaired extinction of cocaine-seeking behavior and associated immune dysregulation in both peripheral and central systems.

This study identifies a DAT-mediated immuno-modulatory mechanism in human macrophages, showing dopamine transport regulates innate immune responses to LPS and is disrupted in disease.