The tumor cells of patients with cutaneous T cell lymphomas (CTCL) have the cell surface phenotype of mature T helper lymphocytes and may be impossible to differentiate from non malignant lymphocytes, both in skin and blood. Until now, no specific cell membrane marker of CTCL has been reported. In the present study, we report for the first time that CTCL cells express the MHC class I binding p140/killer cell immunoglobulin-like receptor which has been described on a minor subset of NK lymphocyte and on a marginal circulating CD8+ T lymphocyte subset. Interestingly, the molecular characterization of this KIR expressed by CTCL allowed us to isolate a novel allelic form of p140/KIR3DL, resulting in four amino acid substitutions, three in the extracellular immunoglobulin-like domain of the protein and one in the cytoplasmic region. This finding is likely to be an important new issue, both for the pathophysiology and for the clinical management of CTCL patients (Blood, 1 March 2001, 97, in press).
Cutaneous T Cell Lymphoma Cells Express a Novel Allelic Form of the p140/Killer Cell Immunoglobulin-Like Receptor
MORETTA, ALESSANDRO;SIVORI, SIMONA;CANTONI, CLAUDIA;BOTTINO, CRISTINA;
2002-01-01
Abstract
The tumor cells of patients with cutaneous T cell lymphomas (CTCL) have the cell surface phenotype of mature T helper lymphocytes and may be impossible to differentiate from non malignant lymphocytes, both in skin and blood. Until now, no specific cell membrane marker of CTCL has been reported. In the present study, we report for the first time that CTCL cells express the MHC class I binding p140/killer cell immunoglobulin-like receptor which has been described on a minor subset of NK lymphocyte and on a marginal circulating CD8+ T lymphocyte subset. Interestingly, the molecular characterization of this KIR expressed by CTCL allowed us to isolate a novel allelic form of p140/KIR3DL, resulting in four amino acid substitutions, three in the extracellular immunoglobulin-like domain of the protein and one in the cytoplasmic region. This finding is likely to be an important new issue, both for the pathophysiology and for the clinical management of CTCL patients (Blood, 1 March 2001, 97, in press).I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.