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

INTRODUCTION

Human T-lymphotropic virus type-1 (HTLV-1) is a retrovirus associated with the development of various diseases. HTLV-1 contributes to the development of several disorders that mimic autoinflammation. The pathogenic processes that underlie the emergence of such auto-inflammation-like conditions following HTLV-1 infection remain a subject of ongoing scientific debate and investigation.

AREAS COVERED: This study provides a comprehensive review of the pathophysiology of HTLV-1-associated inflammatory diseases with an emphasis on the role of regulatory T cells and the plasticity of these cells in the development of such diseases through a selection of the most relevant and recent papers in PubMed and the Web of Science database.

EXPERT OPINION: 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 THAMs. 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.