Immunological status in PBMCs from patients with mogamulizumab-induced EM. After treatment with lymphocyte-depleting mogamulizumab, robust homeostatic CD8⁺ T-cell proliferation occurs, which is driven by the engagement of self-antigens, including skin-related antigens, together with prolonged Treg depletion. This is enhanced by the observed activation of antigen presentation and accompanied by diversification of the TCR repertoire. This proliferation and diversification are primarily the result of newly emergent T-cell clone proliferation at the time of EM development. Subsequently, certain CD8⁺ T cells migrate to the skin and attack it by releasing GZMK and GZMA. Additionally, Th17 cells play an important role in EM, and B cells are activated and differentiate, leading to the production of autoantibodies that attack the skin. APC, antigen-presenting cell; eTreg, effector regulatory T cells; IgG, immunoglobulin G; IgM, immunoglobulin M.