title: Constitutive and induced IL-18 receptor expression by various peripheral blood cell subsets as determined by anti-hIL-18R monoclonal antibody.
abstract: Interleukin-18 (IL-18) was identified as a molecule that induces IFN-gamma production and enhances NK cell cytotoxicity. Characterization of the receptor for human IL-18 (hIL-18R) is important for investigating the physiological role of IL-18 in nature. In the present study, we describe a monoclonal antibody (mAb) against hIL-18R (mAb No. 117-10C). This mAb inhibited the binding of 125I-labeled hIL-18 to IL-18R-expressing L428 cells. This mAb also neutralized hIL-18-induced T helper 1 type cytokine (IFN-gamma and GM-CSF) production by Con A-stimulated PBMC. PBMC were examined for the expression of IL-18R by two-color flow cytometry. Most CD19(+) B cells and a percentage of CD8(+) T cells were found to constitutively express IL-18R. Treatment of PBMC with IL-12 preferentially induced IL-18R expression on CD56(+) NK cells regardless of costimulation with mitogen. IL-18R expression on CD4(+) T cells was induced weakly by IL-12 treatment and moderately by PHA stimulation. However, neither could IL-12 treatment nor PHA stimulation induce IL-18R expression on CD8(+) T cells. Costimulation with both IL-12 and PHA was necessary for optimal IL-18R expression on CD8(+) T cells as well as on CD56(+) NK cells, CD4(+) T cells, and CD19(+) B cells. These results support the growing number of reports showing that IL-18 has modulatory effects on T, B, and NK cells.
authors.affiliation: Fujisaki Institute, Hayashibara Biochemical Laboratories, Inc., Okayama, 702-8006, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Kunikata
authors.forename: K
authors.initials: K
authors.lastname: Torigoe
authors.forename: S
authors.initials: S
authors.lastname: Ushio
authors.forename: T
authors.initials: T
authors.lastname: Okura
authors.forename: C
authors.initials: C
authors.lastname: Ushio
authors.forename: H
authors.initials: H
authors.lastname: Yamauchi
authors.forename: M
authors.initials: M
authors.lastname: Ikeda
authors.forename: H
authors.initials: H
authors.lastname: Ikegami
authors.forename: M
authors.initials: M
authors.lastname: Kurimoto
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology*; D019002:CD56 Antigen / Q000032:analysis; D019556:COS Cells; D002478:Cells, Cultured; D006801:Humans; D018664:Interleukin-12 / Q000494:pharmacology; D053727:Interleukin-18 Receptor alpha Subunit; D007694:Killer Cells, Natural / Q000737:chemistry; D007963:Leukocytes, Mononuclear / Q000737:chemistry*; D051379:Mice; D008807:Mice, Inbred BALB C; D018123:Receptors, Interleukin / Q000032:analysis* / Q000276:immunology; D053724:Receptors, Interleukin-18
chemical_list: D000911:Antibodies, Monoclonal; D019002:CD56 Antigen; C508572:IL18R1 protein, human; C508573:Il18r1 protein, mouse; D053727:Interleukin-18 Receptor alpha Subunit; D018123:Receptors, Interleukin; D053724:Receptors, Interleukin-18; D018664:Interleukin-12