title: Demonstration of a cross-talk between IL-2 and IL-5 in phosphorylation of IL-2 and IL-5 receptor beta chains.
abstract: We have examined phosphorylation mediated by cross-talk between growth signal pathways induced by IL-2 and IL-5. To analyze the phosphorylation process in the same cells, we established two sublines, T88-Mbeta1, which is a subline of a murine IL-5-dependent cell line, T88-M, by introduction of the human IL-2 receptor beta chain (IL-2Rbeta), and secondly CTLL-5Ralphabeta, which is a subline of a murine IL-2-dependent cell line, CTLL-2, by introduction of the murine IL-5 receptor alpha chain (IL-5Ralpha) and IL-5 receptor beta chain (IL-5Rbeta, betac) genes. Both T88-Mbeta1 and CTLL-5Ralphabeta expressed high-affinity receptors for IL-2 and IL-5, and proliferated in response to both factors. Tyrosine phosphorylation of IL-2Rbeta was induced by stimulation of T88-Mbeta1 with not only IL-2 but also IL-5. Anti-IL-2Rbeta-directed immune complexes from T88-Mbeta1 stimulated with IL-5 as well as with IL-2 contained an activated tyrosine kinase. However, stimulation with IL-5 but not IL-2 induced the tyrosine phosphorylation of IL-5Rbeta, betac, suggesting that IL-2 does not activate a tyrosine kinase which efficiently catalyzes the IL-5Rbeta molecule in response to IL-5. On the other hand, the detection of JAK1 and the other common set of phosphotyrosine-containing proteins after stimulation with either IL-5 or IL-2 suggests the existence of the same tyrosine phosphorylation pathways.
authors.affiliation: Department of Microbiology, Tohoku University School of Medicine, 2-1 Seiryo-machi, Sendai 980-77, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Ohbo
authors.forename: H
authors.initials: H
authors.lastname: Asao
authors.forename: T
authors.initials: T
authors.lastname: Kouro
authors.forename: M
authors.initials: M
authors.lastname: Nakamura
authors.forename: S
authors.initials: S
authors.lastname: Takaki
authors.forename: Y
authors.initials: Y
authors.lastname: Kikuchi
authors.forename: K
authors.initials: K
authors.lastname: Hirokawa
authors.forename: A
authors.initials: A
authors.lastname: Tominaga
authors.forename: K
authors.initials: K
authors.lastname: Takatsu
authors.forename: K
authors.initials: K
authors.lastname: Sugamura
mesh_terms: D000818:Animals; D002455:Cell Division / Q000276:immunology; D002460:Cell Line; D007376:Interleukin-2 / Q000494:pharmacology*; D015848:Interleukin-5 / Q000494:pharmacology*; D053613:Janus Kinase 1; D053614:Janus Kinase 2; D053616:Janus Kinase 3; D007700:Kinetics; D051379:Mice; D010766:Phosphorylation / Q000187:drug effects; D011505:Protein-Tyrosine Kinases / Q000032:analysis / Q000378:metabolism; D011518:Proto-Oncogene Proteins; D018123:Receptors, Interleukin / Q000096:biosynthesis / Q000378:metabolism*; D015375:Receptors, Interleukin-2 / Q000096:biosynthesis / Q000378:metabolism*; D053649:Receptors, Interleukin-5; D013602:T-Lymphocytes, Cytotoxic / Q000201:enzymology
chemical_list: D007376:Interleukin-2; D015848:Interleukin-5; D011518:Proto-Oncogene Proteins; D018123:Receptors, Interleukin; D015375:Receptors, Interleukin-2; D053649:Receptors, Interleukin-5; D011505:Protein-Tyrosine Kinases; C507904:JAK1 protein, human; C507924:JAK2 protein, human; C507933:JAK3 protein, human; C507905:Jak1 protein, mouse; C507926:Jak2 protein, mouse; C507935:Jak3 protein, mouse; D053613:Janus Kinase 1; D053614:Janus Kinase 2; D053616:Janus Kinase 3