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Molecular and Cellular Biology, December 2002, p. 8199-8203, Vol. 22, No. 23
0270-7306/02/$04.00+0 DOI: 10.1128/MCB.22.23.8199-8203.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
and Michel C. Nussenzweig1,3*
Laboratory of Molecular Immunology, The Rockefeller University,1 Howard Hughes Medical Institute, New York, New York 10021,3 Department of Medical and Molecular Parasitology, New York University School of Medicine, New York, New York 100102
Received 15 March 2002/ Returned for modification 16 April 2002/ Accepted 16 July 2002
To examine the physiological functions of mannose-binding lectin A (MBL-A), we generated mice that were deficient in MBL-A and examined their susceptibilities to the microbial pathogens Candida albicans and Plasmodium yoelii, an accepted experimental malaria model in mouse. We found no differences in the survival rates and fungal burdens of wild-type and MBL-A-/- mice with disseminated C. albicans infection. The two mouse strains were also similar in their abilities to resist hepatic accumulation of P. yoelii parasites. We conclude that MBL-A deficiency does not alter resistance to disseminated candidiasis or initial hepatic invasion by P. yoelii.
Present address: Division of Hepatology and Gene Therapy, University Clinic and Medical School, University of Navarra, Pamplona, Spain.
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