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Infection and Immunity, September 2002, p. 5304-5306, Vol. 70, No. 9
0019-9567/02/$04.00+0 DOI: 10.1128/IAI.70.9.5304-5306.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Center for Microbial Pathogenesis,1 Departments of Pathology,2 Physiology,3 Medicine,5 Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, Connecticut 06030,6 Division of Infectious Diseases, Connecticut Children's Medical Center, Hartford, Connecticut 061064
Received 14 March 2002/ Returned for modification 25 May 2002/ Accepted 8 June 2002
A new strain of Babesia microti (KR-1) was isolated from a Connecticut resident with babesiosis by hamster inoculation and adapted to C3H/HeJ and BALB/c mice. To examine the relative importance of humoral and cellular immunity for the control of B. microti infection, we compared the course of disease in wild-type BALB/c mice with that in BALB/c SCID mice, JHD-null (B-cell-deficient) mice, and T-cell receptor
ß (TCRß-/-) or gamma interferon (IFN-
) (IFN-
-/-) knockout mice following inoculation with the KR-1-strain. SCID mice and TCR
ß knockouts sustained a severe but nonlethal parasitemia averaging 35 to 45% infected erythrocytes. IFN-
-deficient mice developed a less severe parasitemia but were able to clear the infection. In contrast, in six of eight JHD-null mice, the levels of parasitemia were indistinguishable from those in the wild-type animals. These data indicate that cellular immunity is critical for the clearance of B. microti in BALB/c mice but that disease resolution can occur even in the absence of IFN-
.
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