title: HL-T, a new cell line derived from HL-60 promyelocytic leukemia cell cultures expressing terminal transferase and secreting suppressor activity.
abstract: 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/10(8) 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 (T beta) probes shows JH to be in the germ-line configuration in both cell lines and the T beta 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.
authors.affiliation: Department of Oncology, Montefiore Medical Center, Bronx, NY 10467.
authors.forename: E
authors.initials: E
authors.lastname: Paietta
authors.forename: R J
authors.initials: RJ
authors.lastname: Stockert
authors.forename: T
authors.initials: T
authors.lastname: Calvelli
authors.forename: P
authors.initials: P
authors.lastname: Papenhausen
authors.forename: S V
authors.initials: SV
authors.lastname: Seremetis
authors.forename: M
authors.initials: M
authors.lastname: Fotino
authors.forename: P H
authors.initials: PH
authors.lastname: Wiernik
authors.forename: L
authors.initials: L
authors.lastname: Chang
authors.forename: F J
authors.initials: FJ
authors.lastname: Bollum
mesh_terms: D002460:Cell Line; D002869:Chromosome Aberrations; D005796:Genes; D006801:Humans; D007158:Immunologic Techniques; D007621:Karyotyping; D015470:Leukemia, Myeloid, Acute / Q000201:enzymology / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology; D010641:Phenotype; D013491:Suppressor Factors, Immunologic / Q000378:metabolism*; D014166:Transferases / Q000378:metabolism*
chemical_list: D013491:Suppressor Factors, Immunologic; D014166:Transferases