Article

Immunologic Research

, Volume 34, Issue 1, pp 1-12

Modulation of nuclear factor-ϰB by human T cell leukemia virus type 1 tax protein

Implications for oncogenesis and inflammation
  • Jean-Marie PeloponeseJr.Affiliated withMolecular Virology Section, Laboratory of Molecular Microbiology National Institute of Allergy and Infectious Diseases, National Institutes of Health
  • , Man Lung YeungAffiliated withMolecular Virology Section, Laboratory of Molecular Microbiology National Institute of Allergy and Infectious Diseases, National Institutes of Health
  • , Kuan-Teh JeangAffiliated withMolecular Virology Section, Laboratory of Molecular Microbiology National Institute of Allergy and Infectious Diseases, National Institutes of Health Email author 

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Abstract

Activation of the nuclear factor kappa B (NF-ϰB) transcription factor family by different stimuli, such as inflammatory cytokines, stress inducers, or pathogens, results in innate and adaptive immunity. While the main function of NF-ϰB is to promote the host's immune response, the NF-ϰB pathway is frequently dysregulated by invading viral pathogens. Human T cell leukemia virus type 1 (HTLV-1) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL) and an inflammatory disease named tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). HTLV-1 encodes an oncoprotein, Tax, which plays a significant role in the initiation of cellular transformation and the elicitation of the host's inflammatory responses. Here, we review current thinking on how Tax may affect both diseases through activation of NF-ϰB signaling.

Key Words

Human T cell leukemia virus (HTLV-1) Adult T cell leukemia (ATL) HTLV-1 Tax NF-ϰB IKK NIK Inflammation