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Molecular and Cellular Biology, July 2002, p. 5173-5181, Vol. 22, No. 14
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.14.5173-5181.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Generation of Mice Deficient for Macrophage Galactose- and N-Acetylgalactosamine-Specific Lectin: Limited Role in Lymphoid and Erythroid Homeostasis and Evidence for Multiple Lectins

Thandi M. Onami,1,2 Meei-Yun Lin,1,2 Dawne M. Page,1,2 Shirley A. Reynolds,1,2 Carol D. Katayama,1,2 Jamey D. Marth,3,4 Tatsuro Irimura,5 Ajit Varki,6,7 Nissi Varki,6,7 and Stephen M. Hedrick1,2*

Molecular Biology Section, Division of Biology,1 Cancer Center,2 Howard Hughes Medical Institute,3 Department of Cellular and Molecular Medicine,4 Department of Medicine,6 Glycobiology Research and Training Center, University of California, San Diego, La Jolla, California 92093,7 Laboratory of Cancer Biology, University of Tokyo, Tokyo 113-8657, Japan5

Received 21 March 2002/ Accepted 2 April 2002

Macrophage receptors function in pattern recognition for the induction of innate immunity, in cellular communication to mediate the regulation of adaptive immune responses, and in the clearance of some glycosylated cells or glycoproteins from the circulation. They also function in homeostasis by initiating the engulfment of apoptotic cells. Evidence has suggested that macrophage receptors function to recognize cells that are destined for programmed cell death but not yet overtly apoptotic. We have examined the function of a macrophage receptor specific for unsialylated glycoproteins, known as the mouse macrophage galactose- and N-acetylgalactosamine-specific lectin (mMGL) (Ii et al., J. Biol. Chem. 265:11295-11298, 1990; Sato et al., J. Biochem. [Tokyo] 111:331-336, 1992; Yamamoto et al., Biochemistry 33:8159-8166, 1994). With targeted disruption, we tested whether mMGL is necessary for macrophage function, controlled thymic development, the loss of activated CD8 T cells, and the turnover of red blood cells. Evidence indicates that mMGL may play a nonessential role in several of these macrophage functions. Experiments are presented that indicate the existence of another galactose- and N-acetylgalactosamine-recognizing lectin distinct from mMGL. This may explain the absence of a strong phenotype in mMGL-deficient mice.

* Corresponding author. Mailing address: Department of Biology, University of California, San Diego, La Jolla, CA 92093-0687. Phone: (858) 534-6269. Fax: (858) 534-5611. E-mail: shedrick{at}ucsd.edu.

Molecular and Cellular Biology, July 2002, p. 5173-5181, Vol. 22, No. 14
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.14.5173-5181.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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