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IL‐16 expression in lymphocytes and microglia in HIV‐1 encephalitis
Author(s) -
Zhao M.L.,
Si Q.,
Lee S. C.
Publication year - 2004
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1046/j.0305-1846.2003.00527.x
Subject(s) - microglia , immunocytochemistry , biology , immunology , central nervous system , neuroglia , macrophage , innate immune system , encephalitis , human brain , inflammation , in vitro , microbiology and biotechnology , neuroscience , immune system , virus , endocrinology , biochemistry
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.