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Infection and Immunity, April 2006, p. 2423-2427, Vol. 74, No. 4
0019-9567/06/$08.00+0 doi:10.1128/IAI.74.4.2423-2427.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Department of Virology and Parasitology, Fujita Health University School of Medicine, Toyoake, Aichi 470-1192, Japan,1 Department of Protozoology, Institute of Tropical Medicine, Nagasaki University, Nagasaki, Nagasaki 852-8523, Japan,2 Department of Pathology, Fujita Health University College, Toyoake, Aichi 470-1192, Japan,3 The Forsyth Institute, Boston, Massachusetts 02115,4 Department of Cell Biology and Neuroscience, Division of Life Sciences, Rutgers University, Piscataway, New Jersey 08854-8082,5 Division of Molecular Immunology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Hokkaido 060-0815, Japan6
Received 25 May 2004/ Returned for modification 26 June 2004/ Accepted 30 December 2005
Osteopontin (OPN) knockout mice (OPN-KO mice) died of Plasmodium chabaudi chabaudi infection, although wild-type (WT) mice had self-limiting infections. OPN was detected in the WT mice at 2 days postinfection. OPN-KO mice produced significantly smaller amounts of interleukin-12 and gamma interferon than WT mice produced. These results suggested that OPN is involved in Th1-mediated immunity against malaria infection.
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