title: TCGF (IL 2)-receptor inducing factor(s). I. Regulation of IL 2 receptor on a natural killer-like cell line (YT cells).
abstract: A continuous cell line (YT cells) with inducible receptor for T cell growth factor (TCGF)/interleukin 2 (IL 2) was established from a 15-yr-old boy with acute lymphoblastic lymphoma and thymoma. YT cells were tetraploid, having 4q+ chromosomal markers, and proliferated continuously in vitro without conditioned medium (CM) or IL 2. They were weakly positive for OKT9, OKT11, and Tac antigen (Ag), a determinant closely associated with the receptor for IL 2 (IL 2-R), and were negative for OKT1, OKT3, OKT4, and OKT8 Ag. YT cells also expressed HNK-1 Ag and Fc receptors for IgG, which are expressed on natural killer (NK) cells. They retained a killing activity against human cell lines, including K562 (myeloid), T, and B cell lines. Unlike Tac Ag/IL 2-R(+) cell lines derived from adult T cell leukemia (ATL), YT cells were negative for HTLV, as proved by Southern blotting with cDNA for viral DNA. The expression of Tac Ag was markedly enhanced in 18 hr, when YT cells were incubated with CM from PHA-stimulated peripheral blood leukocytes (PBL) or spleen cells, as determined by immunofluorescence by using flow cytometry and binding assay with 125I-anti-Tac antibody (Ab). The binding study with 125I-labeled recombinant IL 2 showed 3.2 X 10(4) IL 2 receptor sites on YT cells precultured with CM. PHA-P and Con A neither agglutinate nor enhance the expression of IL 2-R/Tac antigen on these non-T cell line cells. Furthermore, neither recombinant IL 2 nor gamma-interferon could induce IL 2-R on YT cells, suggesting the presence of a unique IL 2-R inducing factor in PBL or spleen CM. Unlike Tac Ag on HTLV(+), ATL-derived cell lines (Hut-102, MT-1, ATL-2), the expression of Tac Ag on YT cells was down-regulated by anti-Tac Ab. The induction of Tac Ag/IL 2-R on YT cells seemed specific, because the enhancement of Tac Ag expression was not associated with that of Ia Ag and T9/transferrin receptor.
authors.forename: J
authors.initials: J
authors.lastname: Yodoi
authors.forename: K
authors.initials: K
authors.lastname: Teshigawara
authors.forename: T
authors.initials: T
authors.lastname: Nikaido
authors.forename: K
authors.initials: K
authors.lastname: Fukui
authors.forename: T
authors.initials: T
authors.lastname: Noma
authors.forename: T
authors.initials: T
authors.lastname: Honjo
authors.forename: M
authors.initials: M
authors.lastname: Takigawa
authors.forename: M
authors.initials: M
authors.lastname: Sasaki
authors.forename: N
authors.initials: N
authors.lastname: Minato
authors.forename: M
authors.initials: M
authors.lastname: Tsudo
mesh_terms: D000293:Adolescent; D000911:Antibodies, Monoclonal / Q000502:physiology; D000954:Antigens, Surface / Q000032:analysis / Q000276:immunology; D002460:Cell Line; D002471:Cell Transformation, Neoplastic; D003470:Culture Media; D017977:Deltaretrovirus / Q000032:analysis; D000939:Epitopes / Q000032:analysis; D006801:Humans; D007376:Interleukin-2 / Q000378:metabolism*; D007621:Karyotyping; D007694:Killer Cells, Natural / Q000378:metabolism*; D007938:Leukemia / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D008297:Male; D010641:Phenotype; D011971:Receptors, Immunologic / Q000096:biosynthesis*; D015375:Receptors, Interleukin-2; D013601:T-Lymphocytes / Q000378:metabolism / Q000648:ultrastructure; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7
chemical_list: D000911:Antibodies, Monoclonal; D000954:Antigens, Surface; D003470:Culture Media; D000939:Epitopes; D007376:Interleukin-2; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7