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

World J Gastroenterol. 2005 Dec 28;11(48):7564-8. doi: 10.3748/wjg.v11.i48.7564.

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.

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Amino Acid Sequence
  • Diseases in Twins
  • Gene Expression Profiling
  • Gene Expression Regulation
  • Hepatitis B virus / immunology*
  • Humans
  • Immunity, Innate
  • Interleukin-18 Receptor alpha Subunit
  • Molecular Sequence Data
  • Proteins / genetics
  • Proteins / physiology*
  • Receptors, Interleukin / genetics
  • Receptors, Interleukin-18

Substances

  • Adaptor Proteins, Signal Transducing
  • IL18R1 protein, human
  • Il18r1 protein, mouse
  • Interleukin-18 Receptor alpha Subunit
  • Proteins
  • Receptors, Interleukin
  • Receptors, Interleukin-18
  • TNFAIP1 protein, human