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Molecular and Cellular Biology, August 2000, p. 5363-5369, Vol. 20, No. 15
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Targeted Inactivation of the Tetraspanin CD37 Impairs T-Cell-Dependent B-Cell Response under Suboptimal Costimulatory Conditions

Klaus-Peter Knobeloch,1 Mark D. Wright,2 Adrian F. Ochsenbein,3 Oliver Liesenfeld,4 Jürgen Löhler,5 Rolf M. Zinkernagel,3 Ivan Horak,1,6,* and Zane Orinska1

Department of Molecular Genetics, Institute of Molecular Pharmacology,1 and Institute of Infection Medicine4 and Benjamin Franklin University Hospital,6 Free University of Berlin, Berlin, and Heinrich Pette Institute, University of Hamburg, Hamburg,5 Germany; The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia2; and Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland3

Received 28 January 2000/Returned for modification 13 March 2000/Accepted 17 April 2000

CD37 is a membrane protein of the tetraspanin superfamily, which includes CD9, CD53, CD63, CD81, and CD82. Many of these molecules are expressed on leukocytes and have been implicated in signal transduction, cell-cell interactions, and cellular activation and development. We generated and analyzed mice deficient for CD37. Despite the high expression of CD37 on cells of the immune system, no changes in development and cellular composition of lymphoid organs were observed in mice lacking CD37. Analyses of humoral immune responses revealed a reduced level of immunoglobulin G1 (IgG1) in the sera of nonimmunized mice and an alteration of responses to T-cell-dependent antigens. Antibody responses to model antigen administered in the absence of adjuvant and to viral infections were generally poor in CD37-deficient mice. These poor antibody responses could be overcome by the immunization of antigen together with adjuvant. These results suggest a role for CD37 in T-cell-B-cell interactions which manifests itself under suboptimal costimulatory conditions.

* Corresponding author. Mailing address: Department of Molecular Genetics, Institute of Molecular Pharmacology, Krahmerstr. 6, 12207 Berlin, Germany. Phone: 49-30-8437-1911. Fax: 49-30-8437-1922. E-mail: horak{at}fmp-berlin.de.

Molecular and Cellular Biology, August 2000, p. 5363-5369, Vol. 20, No. 15
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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