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Mechanism of HIV‐1‐TAT induction of interleukin‐1β from human monocytes: Involvement of the phospholipase C/protein kinase C signaling cascade
Author(s) -
Yang Yongbo,
Wu Jianguo,
Lu Yuanan
Publication year - 2010
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.21720
Subject(s) - signal transduction , phosphorylation , biology , protein kinase c , cytokine , kinase , microbiology and biotechnology , immune system , interleukin 19 , monocyte , transcription factor , interleukin , immunology , gene , biochemistry , interleukin 5
Human immunodeficiency virus TAT plays an important role in the disregulation of cytokine production associated with the neurological disorders that follow HIV infection. IL‐1β is one of the important inflammatory cytokines secreted by immune‐activated monocytes/macrophages. Previous reports have shown that extracellular TAT stimulates IL‐1β expression in monocytes/macrophages. However, little is known about the mechanisms and possible TAT‐responsive elements within the IL‐1β promoter. The present study shows that TAT increases the production of IL‐1β in human monocytes; PLC‐PKC pathway‐dependent phosphorylation of p44/42 and JNK MAP kinases participates partially in IL‐1β induction by TAT; specific C/EBP and NF‐κB transcription factor binding elements within the IL‐1β promoter are involved in TAT regulation of IL‐1β production. This study identifies a signaling mechanism for HIV‐1‐induced IL‐1β production in human monocytes that may be involved in the neuropathogenesis of HIV‐associated dementia. J. Med. Virol. 82: 735–746, 2010. © 2010 Wiley‐Liss, Inc.