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IL-16 expression in lymphocytes and microglia in HIV-1 encephalitis
1Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Insights
Interleukin-16 (IL-16) is expressed by brain immune cells in HIV-1 encephalitis. This finding suggests IL-16 modulates inflammation and viral activity in the central nervous system.
Area of Science:
- Neuroimmunology
- Virology
- Cellular Biology
Background:
- Interleukin-16 (IL-16) is a cytokine known to interact with the CD4 molecule.
- IL-16 exhibits chemotactic properties and has demonstrated anti-HIV-1 activity.
- The role of IL-16 in the context of HIV-1 infection within the human brain remains to be fully elucidated.
Purpose of the Study:
- To investigate the expression and cellular localization of IL-16 in human brain tissue affected by HIV-1 encephalitis.
- To determine the cellular sources of IL-16 production in the brain under HIV-1 infection.
- To explore the regulation of microglial IL-16 release by HIV-1.
Main Methods:
- Specific immunocytochemistry was employed to detect IL-16 expression in post-mortem human brain tissue.
- In vitro studies utilized human fetal microglia and astrocytes.
- HIV-1 infection and manipulation of viral Nef expression were used to assess regulation of IL-16 release.
Main Results:
- IL-16 expression was identified in infiltrating lymphocytes and activated microglia within HIV-1 encephalitis brain tissue.
- IL-16 immunoreactivity was notably concentrated in microglial nodules.
- Human fetal microglia, but not astrocytes, were found to produce IL-16, with HIV-1 infection up-regulating its release in a Nef-dependent manner.
Conclusions:
- IL-16 functions as a macrophage-lineage specific modulator of the inflammatory response and HIV-1 expression within the brain.
- The recruitment of IL-16-expressing T cells and microglia/macrophages may represent an innate immune response to HIV-1 in the CNS.
- This innate response potentially counterbalances pro-viral factors in the central nervous system.
Abstract:
IL-16 is a natural ligand for the CD4 molecule and is known for its chemotactic and anti-HIV-1 activities. We determined IL-16 expression in human brain tissue with HIV-1 encephalitis by specific immunocytochemistry and showed that infiltrating lymphocytes and activated microglia express IL-16. IL-16 immunoreactivity was particularly pronounced in microglial nodules. In vitro, human foetal microglia and not astrocytes produce IL-16, and HIV-1 infection up-regulates microglial IL-16 release in a Nef-dependent manner. These results support the notion that, in the brain, IL-16 is a macrophage-lineage specific modulator of the inflammatory response and HIV-1 expression. Recruitment of IL-16+ T cells and microglia/macrophages may represent an innate response to HIV-1 infection in the central nervous system that counterbalances viral stimulatory factors.
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