Mechanism of HIV-1-TAT induction of interleukin-1beta from human monocytes: Involvement of the phospholipase C/protein kinase C signaling cascade.

Human immunodeficiency virus TAT plays an important role in the disregulation of cytokine production associated with the neurological disorders that follow HIV infection. IL-1beta is one of the important inflammatory cytokines secreted by immune-activated monocytes/macrophages. Previous reports have shown that extracellular TAT stimulates IL-1beta expression in monocytes/macrophages. However, little is known about the mechanisms and possible TAT-responsive elements within the IL-1beta promoter. The present study shows that TAT increases the production of IL-1beta in human monocytes; PLC-PKC pathway-dependent phosphorylation of p44/42 and JNK MAP kinases participates partially in IL-1beta induction by TAT; specific C/EBP and NF-kappaB transcription factor binding elements within the IL-1beta promoter are involved in TAT regulation of IL-1beta production. This study identifies a signaling mechanism for HIV-1-induced IL-1beta production in human monocytes that may be involved in the neuropathogenesis of HIV-associated dementia. (c) 2010 Wiley-Liss, Inc.

Citation

Yongbo Yang, Jianguo Wu, Yuanan Lu. Mechanism of HIV-1-TAT induction of interleukin-1beta from human monocytes: Involvement of the phospholipase C/protein kinase C signaling cascade. Journal of medical virology. 2010 May;82(5):735-46

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PMID: 20336759

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