Regulatory T cell plasticity and immune deviation toward autoinflammation in HTLV-1-associated diseases: insights and implications

Recent evidence suggests that HTLV-1 infection induces the expansion of regulatory T cells (Tregs) with high plasticity, which can convert into effector T cells that promote immune deviation toward autoinflammation, including T-helper1 (Th1) cells, T-helper17 (Th17) cells and a novel effector T helper cell subpopulation with particular specificity for HAM/TSP called T_HAMs. The development of novel therapeutic strategies targeting these cells paves the way for new therapeutic strategies, which hold significant promise for providing more favorable treatment outcomes for involved individuals and ameliorating patients' symptoms.