Fig. 1

Potential relationship between innate and acquired immunity in HTLV-1 infection (under IL-10-dominant conditions). The hypothesis describing the possible interaction between persistently HTLV-1-infected cells and host immunity is schematically shown. Although HTLV-1 Tax has a strong ability to activate NFκB, type-I IFNs can suppress Tax expression through ISG at a post-transcriptional level. Intrinsic PAMPs (such as viral RNA) might activate PRRs that largely overlap with ISG and potentially suppress Tax expression while activating NFκB. The microenvironmental cytokine balance could be one of the determinants to polarize the feature of HTLV-1-infected cells towards either proliferation or inflammation. This schematic shows the situation where IL-10 dominates. NFκB together with IL-10-mediated STAT3 positive feedback loop induces IRF4, etc. to promote cell proliferation. For acquired immunity, because of the scarcity of Tax expression in vivo, Tax-specific CTLs may eliminate only a limited number of HTLV-1 infected cells, but still contribute to immune surveillance. However, this surveillance becomes increasingly insufficient when CTL function is impaired by immune tolerance and T-cell exhaustion, which may be accelerated by IL-10, TGF-β, IFNs, and Tregs