Despite the limitations of the study, particularly the sample size, the data we produced on the reduced CSF concentration of TGF-β1 in HTLV-1 infection and increased IL-18 in the CSF of HAM/TSP patients with active neuroinflammation indicate that unbalanced suppressive responses and inflammasome-mediated mechanisms in the CNS might contribute to HAM/TSP development. Here, IL18 is linked to tropical spastic paraparesis.