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Infection and Immunity, January 1999, p. 446-448, Vol. 67, No. 1
Department of Medical Microbiology and
Immunology, University of Wisconsin Medical School, Madison, Wisconsin
Received 15 June 1998/Returned for modification 23 July
1998/Accepted 28 September 1998
Mice depleted of
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

T-Cell Function in Pathogenesis of Cerebral
Malaria in Mice Infected with Plasmodium berghei
ANKA


T cells by monoclonal antibody treatment
and infected with Plasmodium berghei ANKA did not develop
cerebral malaria (CM). In striking contrast,
0/0 mice
infected with P. berghei developed CM despite their 
T-cell deficiency. 
T cells appear to be essential for the
pathogenesis of CM in mice having experienced normal ontogeny but not
in mice genetically deprived of 
T cells from the beginning of life.
*
Corresponding author. Mailing address: Department of
Medical Microbiology and Immunology, University of Wisconsin
Madison, 436 Service Memorial Institutes, 1300 University Ave., Madison, WI
53706. Phone: (608) 262-9027. Fax: (608) 262-8418. E-mail: wweidanz{at}macc.wisc.edu.
Present address: Department of Microbiology and Immunology,
Louisiana State University Medical Center, Shreveport, LA 71103.
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