Table 3 Mechanistic basis of treatments used for the treatment of ATLL.

IFN

• Preventing targeting of viral Gag proteins to the rafts in the plasma membrane

• Induction of 2′-5′oligoadenylate synthase and protein kinase P1

• Stimulation of natural killer cells and macrophages and enhancing antigen presentation to lymphocytes.

• Activation of Jak1 and Tyk2, which lead to induction of tyrosine phosphorylation of the eIF2alpha kinase PKR

AZT

• Inhibition of the reverse transcriptase of the HTLV-1 virus

• Inhibition of telomerase which results in progressive telomere shortening and activation and stabilization of TTP53 in ATLL cases

IFN + ARS

• A rapid shutdown of the NF-kappa B pathway results in the induction of cell cycle arrest and apoptosis

• Restoring PML nuclear body formation

Mogamulizumab

• Targeting CCR4, which is a chemokine receptor that is preferentially expressed by Th2 and regulatory T cells which lead to promoting T-cell migration