Skip to main content

HTLV-1 bZIP factor perturbs immune response to the pathogens in vivo by inhibiting IFN-gamma production

HTLV-1 carriers and the patients with adult T-cell leukemia (ATL) frequently suffer from the opportunistic infections. Although it has been known that HTLV-1 infection evokes cell-mediated immune deficiency, its mechanism remains unknown. HTLV-1 bZIP factor (HBZ) is encoded in the minus strand of HTLV-1, which is constitutively expressed and involved in the proliferation of HTLV-1-infected cells. In this study, we investigated the role of HBZ in immunodeficiency in a mice model. HBZ transgenic (HBZ-Tg) mice were infected with HSV-2 and Listeria monocytogenes and evaluated for cellular immunity to those pathogens. The clearance of both pathogens was impaired in HBZ-Tg mice compared with the non-transgenic littermate. In the both infection, production of IFN-gamma in CD4+ T cells was significantly reduced in HBZ-Tg mice. In addition, ectopic expression of HBZ in primary human CD4+ T cells impaired IFN-gamma production in vitro. As the molecular mechanisms, we found that HBZ suppressed transcription of IFNG promoter. Our results suggest that HBZ plays a crucial role for cellular immunodeficiency in HTLV-1-infected subjects.

Author information

Affiliations

Authors

Corresponding author

Correspondence to Masao Matsuoka.

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Sugata, K., Satou, Y., Yasunaga, J. et al. HTLV-1 bZIP factor perturbs immune response to the pathogens in vivo by inhibiting IFN-gamma production. Retrovirology 8, A102 (2011). https://doi.org/10.1186/1742-4690-8-S1-A102

Download citation

Keywords

  • Leukemia
  • Mouse Model
  • Opportunistic Infection
  • Ectopic Expression
  • Listeria