HL-T, A New Cell Line Derived From HL-60 Promyelocytic Leukemia Cell Cultures Expressing Terminal Transferase and Secreting Suppressor Activity

• Published in: Blood Vol. 70; no. 4; pp. 1151 - 1160
• Main Authors: Paietta, Elisabeth, Stockert, Richard J., Calvelli, Theresa, Papenhausen, Peter, Seremetis, Stephanie V., Fotino, Marilena, Wiernik, Peter H., Chang, Lucy, Bollum, Fred J.
• Format: Journal Article
• Language: English
• Published: Washington, DC Elsevier Inc 01.10.1987; The Americain Society of Hematology
• Subjects: Biological and medical sciences; Cell Line; Chromosome Aberrations; Genes; Hematologic and hematopoietic diseases; Humans; Immunologic Techniques; Karyotyping; Leukemia, Myeloid, Acute - enzymology; Leukemia, Myeloid, Acute - genetics; Leukemia, Myeloid, Acute - pathology; Leukemia, Myeloid, Acute - physiopathology; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis; Medical sciences; Phenotype; Suppressor Factors, Immunologic - metabolism; Transferases - metabolism; DNA nucleotidylexotransferase; Human; Immunohistochemistry; Promyelocytic leukemia; Phenotype; Established cell line; T-Lymphocyte; Cytogenetics; Suppressive cell; Hemopathy; Experimental study; Tumor cell
• ISSN: 0006-4971; 1528-0020
• DOI: 10.1182/blood.V70.4.1151.1151

A cell line with immature blast cell morphology was isolated from HL-60 promyelocytic leukemia cell cultures and designated HL-T. This new cell type is biphenotypic, expressing terminal transferase (TdT) together with myelomonocytoid immunologic features. TdT enzymatic activity, undetectable in HL-60, was determined to be 140 to 180 units/108 HL-T cells by the dGTP-assay, approximately 20% of the activity found in lymphoblastoid cell lines. HL-T predominantly synthesize the known 58-kDa TdT-protein plus a minor 54/56-kDa doublet. The 58-kDa steady state form is nonglycosylated and is phosphorylated. Precursor antigens S3.13 and MY-10, absent on HL-60, are expressed by HL-T; however, the cells are negative for HLA-DR. Southern blot analysis by hybridization with immunoglobulin heavy chain (JH) and T cell-receptor chain gene (Tβ) probes shows JH to be in the germ-line configuration in both cell lines and the Tβ gene to be in germ-line in HL-60 but to be rearranged in HL-T. Truncation of the gene encoding the granulocyte-macrophage–colony-stimulating factor (GM-CSF), as found in HL-60, is not observed in HL-T. HL-T are resistant to differentiation-induction by retinoic acid and 1,25-dihydroxyvitamin D3. Cytogenetically HL-T share with HL-60 a deletion of the short arm of chromosome 9 at breakpoint p13, an aberration frequently found in patients with T cell leukemia. In addition, HL-T display t(8;9)(p11;p24) and trisomy 20. Tetraploidy is observed in 80% of HL-T metaphases with aberrations identical to those in the diploid karyotype. Like HL-60, the new line shows some surface-antigenic–T cell characteristics. Despite an antigenic pattern most consistent with that of helper-inducer T cells (T4+, D44±, 4B4+, 2H4–,TQ1±), HL-T cells and their conditioned culture medium suppress antigen, mitogen, and mixed-leukocyte–culture-mediated lymphocyte proliferation.