Postnatally Induced Inactivation of gp130 in Mice Results in Neurological, Cardiac, Hematopoietic, Immunological, Hepatic, and Pulmonary Defects

doi:10.1084/jem.188.10.1955

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J. Exp. Med., Volume 188, Number 10, November 16, 1998 1955-1965

Postnatally Induced Inactivation of gp130 in Mice Results in Neurological, Cardiac, Hematopoietic, Immunological, Hepatic, and Pulmonary Defects

By Ulrich A.K. Betz,^* Wilhelm Bloch, Maries van den Broek,^§ Kanji Yoshida, Tetsuya Taga,^** Tadamitsu Kishimoto,^¶ Klaus Addicks, Klaus Rajewsky,^* and Werner Müller^*

From the ^* Institute for Genetics and the 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 inhibitoryfactor, oncostatin M, ciliary neurotrophic factor, and cardiotrophin1 are mediated by the cytokine receptor subunit gp130 as the commonsignal transducer. Although mice lacking individual members ofthis family display only mild phenotypes, animals lacking gp130are not viable. To assess the collective role of this cytokinefamily, we inducibly inactivated gp130 via Cre-loxP-mediated recombinationin vivo. Such conditional mutant mice exhibited neurological,cardiac, hematopoietic, immunological, hepatic, and pulmonarydefects, demonstrating the widespread importance of gp130-dependentcytokines.

Key words: gene targeting; conditional gene targeting; Cre/loxP technology; gp130-dependent cytokines; gp130

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