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Institute for Anatomy I, University of Cologne, D-50931 Cologne, Germany; the Institute for Experimental Immunology, University of Zürich, CH-8093 Zürich, Switzerland; the || Department of Molecular Immunology, Research Institute for Microbial Diseases, and the ¶ Department of Medicine III, Medical School, Osaka University, Osaka 565, Japan; and the ** Department of Molecular Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 101, Japan
The pleiotrophic but overlapping functions of the cytokine family that includes interleukin (IL)-6, IL-11, leukemia inhibitory factor, oncostatin M, ciliary neurotrophic factor, and cardiotrophin 1 are mediated by the cytokine receptor subunit gp130 as the common signal transducer. Although mice lacking individual members of this family display only mild phenotypes, animals lacking gp130 are not viable. To assess the collective role of this cytokine family, we inducibly inactivated gp130 via Cre-loxP–mediated recombination in vivo. Such conditional mutant mice exhibited neurological, cardiac, hematopoietic, immunological, hepatic, and pulmonary defects, demonstrating the widespread importance of gp130-dependent cytokines.
Key Words: gene targeting • conditional gene targeting • Cre/loxP technology • gp130-dependent cytokines • gp130
U.A.K. Betz's present address is Pharma Research Antiinfectives, Bayer AG, D-42096 Wuppertal, Germany.
Abbreviations used: APP, acute phase protein(s); CNTF, ciliary neurotrophic factor; CT-1, cardiotrophin 1; JAK, Janus kinase; LIF, leukemia inhibitory factor; MAPK, mitogen-activated protein kinase; OSM, oncostatin M; s, soluble; SAP, serum amyloid P; STAT, signal transducer and activator of transcription; VSV, vesicular stomatitis virus.
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