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Human T cell leukemia virus type I Tax activates CD40 gene expression via the NF-kappa B pathway
Journal article   Open access   Peer reviewed

Human T cell leukemia virus type I Tax activates CD40 gene expression via the NF-kappa B pathway

Edward W Harhaj, Nicole S Harhaj, Christian Grant, Kate Mostoller, Timothy Alefantis, Shao-Cong Sun and Brian Wigdahl
Virology (New York, N.Y.), v 333(1), pp 145-158
2005
PMID: 15708600
url
https://doi.org/10.1016/j.virol.2004.12.008View
Published, Version of Record (VoR) Open

Abstract

NF-kappa B pathway CD40 Human T cell leukemia virus type I
The human T cell leukemia virus type I (HTLV-I) is an oncogenic retrovirus that is etiologically linked to the genesis of adult T cell leukemia (ATL) as well as HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Emerging evidence suggests that the pathogenicity of HTLV-I involves deregulated activation of immune cells, especially T lymphocytes, although the underlying mechanism remains unclear. In this study, we demonstrate that HTLV-I Tax induces the aberrant expression of CD40, a member of the tumor necrosis factor receptor (TNFR) family that plays an important role in lymphocyte activation and differentiation. In a panel of HTLV-I-transformed T cell lines analyzed, CD40 expression was highly elevated compared to HTLV-I-negative T cells. Using Tax mutants and a genetically manipulated T cell system, we demonstrated that Tax-induced CD40 expression required the NF-κB signaling pathway. In addition, ligation of CD40 on T cells with recombinant CD40L elicited NF-κB activation, suggesting that the CD40 pathway is intact and may participate in a positive regulatory loop in T cells. CD40 ligation strongly synergized with Tax to activate NF-κB, suggesting that CD40 signals may costimulate Tax-mediated NF-κB activation, particularly when Tax is expressed at low levels. Collectively, these results indicate that CD40 is a novel Tax-regulated gene, and the regulation of CD40 by Tax may play a role in cellular activation and HTLV-I-induced disease pathogenesis.

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Collaboration types
Domestic collaboration
Web of Science research areas
Virology
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