title: Lymphokine-regulated differential expression of mRNA for p75kDa-IL-2R and p55kDa-IL-2R in a cloned B lymphoma line (BLC1-CL-3 cells).
abstract: IL-5 renders BCL1-CL-3 (CL-3) cells responsive to IL-2 by increasing the number of high affinity IL-2R, whereas IL-4 prohibits such action of IL-5 to prepare CL-3 cells responsive to IL-2. Here we have found that genes for p75kDa-IL-2R and p55kDa-IL-2R are differentially regulated by IL-4 and IL-5. Nonstimulated CL-3 cells constitutively express mRNA for p75kDa-IL-2R and p55kDa-IL-2R. IL-5 stimulation principally augments the expression of p75kDa-IL-2R mRNA (4- to 8-fold), although modestly increasing the expression of p55kDa-IL-2R mRNA. Kinetic studies have revealed a maximal increase in p75kDa-IL-2R mRNA expression at 12 h and a decline thereafter, substantiating our previous kinetic study of the expression of high affinity IL-2R after the IL-5 stimulation. By contrast, IL-4 stimulation modestly increases the expression of p75kDa-IL-2R mRNA, whereas markedly reducing the expression of p55kDa-IL-2R mRNA, irrespective of whether CL-3 cells were stimulated with IL-4 alone or together with IL-5 and IL-2. Moreover, addition of IL-4 into the culture containing IL-5 and IL-2 causes striking reduction in the level of J-chain mRNA, which otherwise is markedly induced by stimulation with IL-5 and IL-2. These results clearly illustrate the differential regulation of p75kDa- and p55kDa-IL-2R-gene expression by IL-5 and IL-4, and reinforce our notion that increased expression of high affinity IL-2R induced by IL-5 is responsible for the IL-2 competent state, and decreased expression of p55kDa-IL-2R by IL-4 is responsible for IL-2 unresponsive state.
authors.affiliation: Third Department of Internal Medicine, Hyogo College of Medicine, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Nakanishi
authors.forename: K
authors.initials: K
authors.lastname: Matsui
authors.forename: S
authors.initials: S
authors.lastname: Hirose
authors.forename: T
authors.initials: T
authors.lastname: Yoshimoto
authors.forename: K
authors.initials: K
authors.lastname: Hiroishi
authors.forename: T
authors.initials: T
authors.lastname: Kono
authors.forename: T
authors.initials: T
authors.lastname: Hada
authors.forename: T
authors.initials: T
authors.lastname: Hamaoka
authors.forename: K
authors.initials: K
authors.lastname: Higashino
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000502:physiology*; D015870:Gene Expression / Q000187:drug effects; D007144:Immunoglobulin J-Chains / Q000235:genetics; D066298:In Vitro Techniques; D015847:Interleukin-4 / Q000494:pharmacology; D015848:Interleukin-5 / Q000494:pharmacology; D007378:Interleukins / Q000494:pharmacology*; D008223:Lymphoma / Q000235:genetics; D046911:Macromolecular Substances; D051379:Mice; D008970:Molecular Weight; D012333:RNA, Messenger / Q000235:genetics; D015375:Receptors, Interleukin-2 / Q000235:genetics*; D013997:Time Factors; D014407:Tumor Cells, Cultured
chemical_list: D007144:Immunoglobulin J-Chains; D015848:Interleukin-5; D007378:Interleukins; D046911:Macromolecular Substances; D012333:RNA, Messenger; D015375:Receptors, Interleukin-2; D015847:Interleukin-4