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Molecular and Cellular Biology, October 2000, p. 7178-7182, Vol. 20, No. 19
0270-7306/00/$04.00+0

Natural Killer Cells and Mast Cells from gp49B Null Mutant Mice Are Functional

Susana Rojo,1 Christopher C. Stebbins,1 Mary E. Peterson,1 David Dombrowicz,2 Nicolai Wagtmann,1,dagger and Eric O. Long1,*

Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852,1 and Centre d'Immunologie et de Biologie Parasitaire, Institut Pasteur de Lille, 245-59019 Lille Cedex, France2

Received 1 June 2000/Accepted 7 July 2000

Immune responses are controlled by a combination of positive and negative cellular signals. Effector cells in the immune system express inhibitory receptors that serve to limit effector cell expansion and to protect the host from autoreactivity. gp49B is a receptor of unknown function that is expressed on activated mast cells and natural killer (NK) cells and whose cytoplasmic tail endows it with inhibitory potential. To gain insight into the function of gp49B in mice, we disrupted the gp49B gene by homologous recombination. gp49B0 mice were born at expected ratios, were healthy and fertile, and displayed normal long-term survival rates. gp49B0 mice showed no defect in NK or mast cell development. Furthermore, NK and mast cells from the gp49B0 mice showed activation properties in vitro similar to those of cells isolated from wild-type mice. Therefore, gp49B is not critical for the development, expansion, and maturation of mast cells and NK cells in vivo. The healthy status of gp49B0 mice makes them suitable for testing the role of gp49B in immune responses to infectious agents.

* Corresponding author. Mailing address: LIG-NIAID-NIH Twinbrook II, 12441 Parklawn Dr., Rockville, MD 20852-1727. Phone: (301) 496-8266. Fax: (301) 402-0259. E-mail: elong{at}nih.gov.

dagger Present address: Novo Nordisk, DK-2880 Bagsvaerd, Denmark.

Molecular and Cellular Biology, October 2000, p. 7178-7182, Vol. 20, No. 19
0270-7306/00/$04.00+0


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