caa a22 4500 469032529 CHVBK 20180323132747.0 cr unu---uuuuu 170328e19920101xx s 000 0 eng 10.1007/BF00216623 doi (NATIONALLICENCE)springer-10.1007/BF00216623 Activation of immunoglobulin control elements in trasgenic mice [Elektronische Daten] [Andra Miller, David Ennist, Keiko Ozato, Heiner Westphal] To assess the role interleukins and mitogens play in regulating immunoglobulin (Ig) gene expression via the Ig enhancer and promoter, transgenic mice carrying two different Ig gene regulatory regions were generated. One, EμkCAT, contains the Ig heavy chain enhancer (Eμ) and the κ light chain promoter driving the chloramphenicol acetyltransferase (CAT) gene. In the other, ΔEμkCAT, CAT is under the control of the κ promoter alone. Eμ and κ relative activity were assessed by CAT assay. In EμkCAT mice, low CAT expression was consistently found in spleen, bone marrow, mesenteric lymph node, and thymus but not in brain, lung, or kidney. In ΔEμkCAT mice, CAT expression was detectable just above background in lymphoid tissues, suggesting a basic level of tissue specificity in the absence of the enhancer. Whole spleen cell cultures prepared from the mice were treated with lymphokines and mitogens. Lipopolysaccharide (LPS), concanavilin A (Con A), interleukin 6 (IL-6), and interferon-γ (IFN-γ) increased CAT expression to varying extents in cells derived from EμkCAT mice but not in spleen cells prepared from EμkCAT mice. Thus, the presence of Eμ, in addition to the ϰ promoter, is essential for the stimulation of CAT expression mediated by these factors. B cells from EμkCAT mice were separated by density into populations of small and large cells. In untreated small B cells, no CAT expression was detected and only addition of LPS resulted in an increase in CAT expression. In large B cells, CAT was expressed at a low level without addition of exogenous factors. Incubation with LPS, IL-6, Con A and IFN-γ caused CAT expression to increase several-fold. This transgenic system provides a means to identify exogenous factors that activate Ig enhancers and promoters. Springer-Verlag, 1992 Miller Andra Laboratories of Mammalian Genes and Development, National Institutes of Health, 20892, Bethesda, MD, USA aut Ennist David Developmental and Molecular Immunity, National Institute of Child Health and Human Development, 20892, Bethesda, MD, USA aut Ozato Keiko Developmental and Molecular Immunity, National Institute of Child Health and Human Development, 20892, Bethesda, MD, USA aut Westphal Heiner Laboratories of Mammalian Genes and Development, National Institutes of Health, 20892, Bethesda, MD, USA aut Immunogenetics Springer-Verlag 35/1(1992-01-01), 24-32 0093-7711 35:1<24 1992 35 251 https://doi.org/10.1007/BF00216623 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00216623 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Miller Andra Laboratories of Mammalian Genes and Development, National Institutes of Health, 20892, Bethesda, MD, USA aut NATIONALLICENCE 700 1- Ennist David Developmental and Molecular Immunity, National Institute of Child Health and Human Development, 20892, Bethesda, MD, USA aut NATIONALLICENCE 700 1- Ozato Keiko Developmental and Molecular Immunity, National Institute of Child Health and Human Development, 20892, Bethesda, MD, USA aut NATIONALLICENCE 700 1- Westphal Heiner Laboratories of Mammalian Genes and Development, National Institutes of Health, 20892, Bethesda, MD, USA aut NATIONALLICENCE 773 0- Immunogenetics Springer-Verlag 35/1(1992-01-01), 24-32 0093-7711 35:1<24 1992 35 251 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer