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Molecular and Cellular Biology, January 2007, p. 595-604, Vol. 27, No. 2
0270-7306/07/$08.00+0     doi:10.1128/MCB.01503-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Normal Lymphatic Development and Function in Mice Deficient for the Lymphatic Hyaluronan Receptor LYVE-1{triangledown} ,{dagger}

Nicholas W. Gale,1,{ddagger} Remko Prevo,2,{ddagger} Jorge Espinosa,2 David J. Ferguson,3 Melissa G. Dominguez,1 George D. Yancopoulos,1 Gavin Thurston,1 and David G. Jackson2*

Regeneron Pharmaceuticals, Inc., 777 Old Saw Mill River Road, Tarrytown, New York 10591,1 MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford OX3 9DS, United Kingdom,2 Nuffield Department of Pathology, John Radcliffe Hospital, Headington, Oxford OX3 9DS, United Kingdom3

Received 12 August 2006/ Returned for modification 19 September 2006/ Accepted 28 October 2006

The hyaluronan receptor LYVE-1 is expressed abundantly on the surfaces of lymphatic vessels and lymph node sinus endothelial cells from early development, where it has been suggested to function both in cell adhesion/transmigration and as a scavenger for hyaluronan turnover. To investigate the physiological role(s) of LYVE-1, we generated mice in which the gene for the receptor was inactivated by replacement with a ß-galactosidase reporter. LYVE-1–/– mice displayed an apparently normal phenotype, with no obvious alteration in lymphatic vessel ultrastructure or function and no apparent change in secondary lymphoid tissue structure or cellularity. In addition, the levels of hyaluronan in tissue and blood were unchanged. LYVE-1–/– mice also displayed normal trafficking of cutaneous CD11c+ dendritic cells to draining lymph nodes via afferent lymphatics and normal resolution of oxazolone-induced skin inflammation. Finally, LYVE-1–/– mice supported normal growth of transplanted B16F10 melanomas and Lewis lung carcinomas. These results indicate that LYVE-1 is not obligatory for normal lymphatic development and function and suggest either the existence of compensatory receptors or a role more specific than that previously envisaged.

* Corresponding author. Mailing address: MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford OX3 9DS, United Kingdom. Phone: 44 1865 222313. Fax: 44 1865 222502. E-mail: djackson{at}hammer.imm.ox.ac.uk.

{triangledown} Published ahead of print on 13 November 2006.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

{ddagger} The contributions of both of these authors should be considered equal.

Molecular and Cellular Biology, January 2007, p. 595-604, Vol. 27, No. 2
0270-7306/07/$08.00+0     doi:10.1128/MCB.01503-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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