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Cutaneous gamma–delta T-cell lymphoma

Cutaneous gamma–delta T-cell lymphoma (CGDTCL) is a rare entity that has been included as a provisional category in the newly revised World Health Organisation–European Organisation for Research and Treatment of Cancer consensus classification for cutaneous lymphomas [1]. This group includes cases previously known as subcutaneous-panniculitic T-cell lymphomas (SPTCL) with a gamma–delta phenotype (comprising *25% of all previously known SPTCL) [2]. We present a case of cutaneous T-cell lymphoma with immunophenotypic features indicative of gamma–delta T-cell origin. An 80-year-old woman presented with eczema and pruritic skin plaques on her extremities and trunk for 4 months. Examination revealed multiple generalised indurated erythematous nodules and ulcerated tumors with central necrotic eschar (Figure 1). She had associated inguinal and axillary lymphadenopathy without hepatosplenomegaly. Laboratory tests revealed a slight anemia with monocytosis, and an elevated lactate dehydrogenase (282 U/L). Skin biopsies were consistent with a primary CGD-TCL, demonstrating an atypical dermal lymphoid infiltrate with epidermotropism. The infiltrate consisted of intermediate to large atypical lymphoid cells with vesicular chromatin, prominent nucleoli, and scant cytoplasm. The immuno-histochemical stains were positive for CD3, CD7 and T-cell intracellular antigen 1 (TIA-1), but negative for CD4, CD8, CD30, CD56 and beta F1. The chromogenic in situ hybridisation for Epstein–Barr virus (EBV) was negative. Flow cytometric immunophenotyping showed predominant CD3 positive lymphoid cells that co-expressed CD7 and gamma–delta T-cell receptor (TCR), but lacked CD4, CD5 and CD8 expression (Table I). The patient declined a bone marrow aspirate. Peripheral blood flow cytometry and screening imaging studies were negative for systemic involvement. The patient elected to receive palliative treatment with hospice care and expired 1 month later. T-cells have the ability to rearrange their genes providing a great diversity of TCRs expressing a heterodimer of either alpha–beta or gamma–delta chains [3] in association with the CD3 complex of proteins on the cell surface [4]. Although the majority of human peripheral blood lymphocytes express the alpha–beta phenotype [5], gamma–delta T-cells are relatively enriched in epithelial tissues and express the TCR-delta variable region 2 gene and are thought to play an important role in immunosurveillance [3]. Additionally, these cells have cytotoxic capabilities and most of them lack CD4 and CD8 surface markers (‘double negative’ phenotype) [3,4]. CGD-TCL is a rare entity and appears to represent a clonal expansion of functionally mature gamma–delta T-cells that express and release cytotoxic proteins TIA-1, granzyme B, and perforin which are capable of inducing cellular apoptosis and necrosis [4]. The underlying etiology of CGD-TCL is unknown; however, Toro et al. [4] suggested that chronic antigen stimulation may play an inciting role. Previous reports suggest that EBV does not play a major role in the development of primary CGD-TCL [4]. There are, however, subsets of EBV-positive GD-TCL that typically arise at mucocutaneous sites,