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Tumor necrosis factor-alpha-induced protein 1 and immunity to hepatitis B virus.

ABSTRACT: AIM:To compare the gene expression profile in a pair of HBV-infected twins. METHODS:The gene expression profile was compared in a pair of HBV-infected twins. RESULTS:The twins displayed different disease outcomes. One acquired natural immunity against HBV, whereas the other became a chronic HBV carrier. Eighty-eight and forty-six genes were found to be up- or down-regulated in their PBMCs, respectively. Tumor necrosis factor-alpha-induced protein 1 (TNF-alphaIP1) that expressed at a higher level in the HBV-immune twins was identified and four pairs of siblings with HBV immunity by RT-PCR. However, upon HBV core antigen stimulation, TNF-alphaIP1 was downregulated in PBMCs from subjects with immunity, whereas it was slightly upregulated in HBV carriers. Bioinformatics analysis revealed a K+ channel tetramerization domain in TNF-alphaIP1 that shares a significant homology with some human, mouse, and C elegan proteins. CONCLUSION:TNF-alphaIP1 may play a role in the innate immunity against HBV.

SUBMITTER: Lin MC

PROVIDER: S-EPMC4727213 | biostudies-literature | 2005 Dec

REPOSITORIES: biostudies-literature

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Tumor necrosis factor-alpha-induced protein 1 and immunity to hepatitis B virus.

Lin Marie C MC Lee Nikki P NP Zheng Ning N Yang Pai-Hao PH Wong Oscar G OG Kung Hsiang-Fu HF Hui Chee-Kin CK Luk John M JM Lau George Ka-Kit GK

World journal of gastroenterology 20051201 48

<h4>Aim</h4>To compare the gene expression profile in a pair of HBV-infected twins.<h4>Methods</h4>The gene expression profile was compared in a pair of HBV-infected twins.<h4>Results</h4>The twins displayed different disease outcomes. One acquired natural immunity against HBV, whereas the other became a chronic HBV carrier. Eighty-eight and forty-six genes were found to be up- or down-regulated in their PBMCs, respectively. Tumor necrosis factor-alpha-induced protein 1 (TNF-alphaIP1) that expre ...[more]

PMID: 16437679

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Project description:Human Immunodeficiency Virus-1 (HIV-1)-associated neurocognitive disorder (HAND) is likely neuroinflammatory in origin, believed to be triggered by inflammatory and oxidative stress responses to cytokines and HIV protein gene products such as the HIV transactivator of transcription (Tat). Here we demonstrate increased messenger RNA for nuclear factor-kappa B (NF-kappaB) family member, transcription factor RelB, in the brain of doxycycline-induced Tat transgenic mice, and increased RelB synthesis in Tat-exposed microglial cells. Since genetic ablation of RelB in mice leads to multi-organ inflammation, we hypothesized that Tat-induced, newly synthesized RelB inhibits cytokine production by microglial cells, possibly through the formation of transcriptionally inactive RelB/RelA complexes. Indeed, tumor necrosis factor-alpha (TNFalpha) production in monocytes isolated from RelB deficient mice was significantly higher than in monocytes isolated from RelB expressing controls. Moreover, RelB overexpression in microglial cells inhibited Tat-induced TNFalpha synthesis in a manner that involved transcriptional repression of the TNFalpha promoter, and increased phosphorylation of RelA at serine 276, a prerequisite for increased RelB/RelA protein interactions. The Rel-homology-domain within RelB was necessary for this interaction. Overexpression of RelA itself, in turn, significantly increased TNFalpha promoter activity, an effect that was completely blocked by RelB overexpression. We conclude that RelB regulates TNFalpha cytokine synthesis by competitive interference binding with RelA, which leads to downregulation of TNFalpha production. Moreover, because Tat activates both RelB and TNFalpha in microglia, and because Tat induces inflammatory TNFalpha synthesis via NF-kappaB, we posit that RelB serves as a cryoprotective, anti-inflammatory, counter-regulatory mechanism for pathogenic NF-kappaB activation. These findings identify a novel regulatory pathway for controlling HIV-induced microglial activation and cytokine production that may have important therapeutic implications for the management of HAND.

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Tumor necrosis factor-alpha-induced protein 1 and immunity to hepatitis B virus.

Publications

Tumor necrosis factor-alpha-induced protein 1 and immunity to hepatitis B virus.

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