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Review
. 2011 Aug;3(8):1374-94.
doi: 10.3390/v3081374. Epub 2011 Aug 8.

HTLV-1 and innate immunity (VSports app下载)

Chloé Journo  1 , Renaud Mahieux
Affiliations
Review

"V体育2025版" HTLV-1 and innate immunity

Chloé Journo et al. Viruses. 2011 Aug.

"V体育ios版" Abstract

Innate immunity plays a critical role in the host response to a viral infection VSports手机版. The innate response has two main functions. First, it triggers effector mechanisms that restrict the infection. Second, it primes development of the adaptive response, which completes the elimination of the pathogen or of infected cells. In vivo, HTLV-1 infects T lymphocytes that participate in adaptive immunity but also monocytes and dendritic cells that are major players in innate immunity. Herein, we will review the interplay between HTLV-1 and innate immunity. Particular emphasis is put on HTLV-1-induced alteration of type-I interferon (IFN-I) function. In vitro, the viral Tax protein plays a significant role in the alteration of IFN synthesis and signaling. Despite this, IFN-I/AZT treatment of Adult T-cell Leukemia/Lymphoma (ATLL) patients leads to complete remission. We will discuss a model in which exogenous IFN-I could act both on the microenvironment of the T-cells to protect them from infection, and also on infected cells when combined with other drugs that lead to Tax down-regulation/degradation. .

Keywords: HTLV-1; dendritic cells; innate immunity; interferon; monocytes; natural killer cells. V体育安卓版.

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Figures

Figure 1.
Figure 1.
Interplay between HTLV-1 and the type-I interferon (IFN-I) induction pathway. A simplified schematic of the TLR-induced IFN-I induction pathway is shown. Recognition of PAMPs by TLR3 induces the recruitment of the adaptor molecule TRIF. TRIF activates via TRAF3 the kinases TBK1 and IKKɛ that phosphorylate IFR3 and IRF7 transcription factors. IRF3/7 heterodimers activate transcription of IFN-I (especially IFN-β). This initial transcription and synthesis wave is followed by a second wave of IFN-α resulting from an amplification loop that involves IRF7. TLR7, 8 and 9, specifically expressed in pDCs, activate IRF7, which stimulates synthesis of IFN-α via MyD88, IRAK1/4 and TRAF6. In vitro, sensing of HTLV-1 induces TLR7-dependent IFN-α secretion by pDCs [59]. However, pDCs isolated from HTLV-1-infected individuals show an altered ability to produce IFN-α in response to viral stimulation (e.g., by HSV-1) [46]. In vitro, HTLV-1 Tax targets IRF3 function, but the data are conflicting: while some indicate an inhibitory effect of Tax mediated by SOCS1-induced IRF3 degradation [67], others show constitutive activation of IRF3 by Tax [68].
Figure 2.
Figure 2.
Alteration of the IFN-I signaling pathway by HTLV-1. Binding of IFN-I on IFNAR-1 and IFNAR-2 IFNAR receptors activates the Jak1 and Tyk2 kinases, which phosphorylate STAT1 and STAT2 proteins. Activated STATs form heterodimers that bind to IRF9 to generate the ISGF3 complex. This complex migrates into the nucleus and activates the transcription of ISGs by recruiting the co-activator CBP/p300. HTLV-1 hinders Tyk2 and STAT2 phosphorylation. Moreover, HTLV-1 Tax interacts with CBP/p300 and inhibits its recruitment by the ISGF3 complex. From data published in [25,27].
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