title: Characteristics of the IL-2 receptor expressed on large granular lymphocytes from patients with abnormally expanded large granular lymphocytes. Implication of a non-Tac IL-2-binding peptide.
abstract: Large granular lymphocytes (LGL) from four patients with abnormally expanded LGL in the peripheral blood were studied regarding their receptor for IL-2. LGL from none of the cases examined expressed Tac Ag, an Il-2R glycoprotein recognized by anti-Tac mAb. However, 125I-labeled IL-2 binding experiments demonstrated that 1400 to 2800/cell IL-2 binding sites with a single affinity (K: 0.46-1.4 nM) were expressed on LGL from the four patients. The affinity was not high but about 10-fold higher than that of the low affinity IL-2R expressed on activated normal T lymphocytes. Furthermore, LGL from the four patients proliferated in response to higher concentrations of IL-2 and these responses were not inhibited by an excess amount of anti-Tac antibody. 125I-Labeled IL-2 cross-linking studies performed in two cases revealed the predominant expression of an IL-2 binding molecule with an estimated Mr of 70,000 to 75,000. After the culture with IL-2 for 48 h, expression of a small amount of Tac Ag (p55) was induced on LGL in at least three cases. These data strongly suggested that the IL-2R expressed on LGL is functional and identical to the p70, a novel IL-2 binding peptide that has been recently identified and speculated to form the high affinity IL-2R in association with the p55.
authors.affiliation: First Division of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Hori
authors.forename: T
authors.initials: T
authors.lastname: Uchiyama
authors.forename: R
authors.initials: R
authors.lastname: Onishi
authors.forename: M
authors.initials: M
authors.lastname: Kamio
authors.forename: H
authors.initials: H
authors.lastname: Umadome
authors.forename: S
authors.initials: S
authors.lastname: Tamori
authors.forename: T
authors.initials: T
authors.lastname: Motoi
authors.forename: T
authors.initials: T
authors.lastname: Kodaka
authors.forename: H
authors.initials: H
authors.lastname: Uchino
mesh_terms: D000328:Adult; D000368:Aged; D000943:Antigens, Differentiation / Q000032:analysis; D000954:Antigens, Surface / Q000032:analysis* / Q000096:biosynthesis; D003432:Cross-Linking Reagents; D005260:Female; D006801:Humans; D007376:Interleukin-2 / Q000378:metabolism* / Q000494:pharmacology; D007694:Killer Cells, Natural / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011971:Receptors, Immunologic / Q000032:analysis* / Q000502:physiology; D015375:Receptors, Interleukin-2; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7
chemical_list: D000943:Antigens, Differentiation; D000954:Antigens, Surface; D003432:Cross-Linking Reagents; D007376:Interleukin-2; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7