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Funding sources: none.

Conflicts of interest: none declared.

Madam, The majority of cell lines derived from mycosis fungoides and Sézary syndrome (SS), representatives of cutaneous T‐cell lymphoma (CTCL), are positive for CD4, and CD8+ cases are rare.1 Here, we established a CD8+CD56+ skin‐infiltrating tumour cell line from skin blisters of a patient with CD8+ SS. Using this cell line, the peculiar features of CD8+ CTCL cells were studied.

The patient’s clinical information has been described elsewhere.2 Briefly, a 26‐year‐old woman had erythroderma with conspicuous blister formation and lymphocytosis (2·5 × 109 cells L−1). Approximately 40% of peripheral blood mononuclear cells (PBMCs) had a CD2highCD3lowCD8+CD56+CLA+CD4 phenotype and expressed CXCR3 at an intermediate level and CCR10 at a high level, but did not express CCR4. CD8+CD56+CLA+ tumour cells infiltrated the skin with marked epidermotropism. Blood and lymph node involvement was confirmed by demonstration of identical clonal rearrangment of the T‐cell receptor Cβ1 gene. After informed consent and approval by the ethical committee of our university, we established a tumour T‐cell line. More than 3 months after termination of substantial treatments, including interferon (IFN)‐γ and radiation, skin‐infiltrating cells were obtained by aspiration of the blister fluid without an invasive procedure, and subsequent purification by Ficoll–Hypaque. Cells were cultured with 10 ng mL−1 interleukin (IL)‐7 in complete RPMI‐1640, and expanded to 200 μL per well in round‐bottom 96‐well plates. Fresh culture medium was added to the well every 2 days, and the cells were collected each week. A long‐term tumour T‐cell line, termed CD8SSC, was established by maintaining it over 6 months. DNAs extracted from a skin specimen and CD8SSC were subjected to Southern blotting analysis for Cβ1 after digestion with BamHI restriction enzyme. The same rearranged nongerm line band was detected in both samples. The patient had no antihuman T‐cell lymphotropic virus 1 (HTLV‐1) antibody, and there was no monoclonal integration of HTLV‐1 proviral DNA into blood or CD8SSC.

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