Interleukin-10 Deficient Mice View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1995

AUTHORS

Jan E. de Vries , René de Waal Malefyt , Donna Rennick , Dan Berg , Ralf Kühn , Werner Müller

ABSTRACT

After the mutation which inactivates the IL-4 gene had been introduced into embryonic stem cells, but before the IL-4-deficient mice1 had been generated or analyzed, a new cytokine, designated interleukin-10 (IL-10) was cloned.2 Many of the biological properties of this new cytokine such as the induction of increased expression of MHC class II molecules on B cells3 and a strong inhibitory effect on the production of inflammatory cytokines by macrophages4,5 were similar to those of IL-4. Consequently, it seemed logical to inactivate the IL-10 gene in the mouse germline to elucidate its main biological functions and in the future to combine the two mutations by crossing the mutant mice. As the entire genomic structure of the IL-10 gene was not known at the time of the gene inactivation construct, we decided to replace a portion of its putative first exon by the neomycin gene and to introduce a frame shift mutation into the coding region by destroying an EcoRI site of the genomic clone a site which was later found to be located in the third exon of the gene.6,7 More... »

PAGES

141-148

Book

TITLE

Interleukin-10

ISBN

978-3-662-22040-5
978-3-662-22038-2

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-3-662-22038-2_16

DOI

http://dx.doi.org/10.1007/978-3-662-22038-2_16

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1021644914


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