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Molecular and Cellular Biology, November 2002, p. 8035-8043, Vol. 22, No. 22
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.22.8035-8043.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Inactivation of the F4/80 Glycoprotein in the Mouse Germ Line

Evelyne Schaller,1 Alison J. Macfarlane,2 Rudolf A. Rupec,3 Siamon Gordon,2 Andrew J. McKnight,2,{dagger} and Klaus Pfeffer1*

Institute of Medical Microbiology, Immunology and Hygiene, Technical University of Munich, D-81675 Munich,1 Department of Dermatology and Allergy, Ludwig-Maximilians-University, D-80337 Munich, Germany,3 Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England2

Received 3 June 2002/ Returned for modification 9 July 2002/ Accepted 20 August 2002

Macrophages play a crucial role in the defense against pathogens. Distinct macrophage populations can be defined by the expression of restricted cell surface proteins. Resident tissue macrophages, encompassing Kupffer cells of the liver and red pulp macrophages of the spleen, characteristically express the F4/80 molecule, a cell surface glycoprotein related to the seven transmembrane-spanning family of hormone receptors. In this study, gene targeting was used to simultaneously inactivate the F4/80 molecule in the germ line of the mouse and to produce a mouse line that expresses the Cre recombinase under the direct control of the F4/80 promoter (F4/80-Cre knock-in). F4/80-deficient mice are healthy and fertile. Macrophage populations in tissues can develop in the absence of F4/80 expression. Functional analysis revealed that the generation of T-cell-independent B-cell responses and macrophage antimicrobial defense after infection with Listeria monocytogenes are not impaired in the absence of F4/80. Interestingly, tissues of F4/80-deficient mice could not be labeled with anti-BM8, another macrophage subset-specific marker with hitherto undefined molecular antigenic structure. Recombinant expression of a F4/80 cDNA in heterologous cells confirmed this observation, indicating that the targets recognized by the F4/80 and BM8 monoclonal antibodies are identical.

* Corresponding author. Mailing address: Institute of Medical Microbiology, Immunology and Hygiene, Technical University of Munich, D-81675 Munich, Germany. Phone: 49 89 4140 4132. Fax: 49 89 4140 4139. E-mail: klaus.pfeffer{at}lrz.tu-muenchen.de.

{dagger} Present address: Celltech R&D Ltd., Slough SL1 4EN, Berkshire, United Kingdom.

Molecular and Cellular Biology, November 2002, p. 8035-8043, Vol. 22, No. 22
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.22.8035-8043.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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