Cellular immunity, but not gamma interferon, is essential for resolution of Babesia microti infection in BALB/c mice

被引:35
作者
Clawson, ML
Paciorkowski, N
Rajan, TV
La Vake, C
Pope, C
La Vake, M
Wikel, SK
Krause, PJ
Radolf, JD
机构
[1] Univ Connecticut, Ctr Hlth, Ctr Microbial Pathogenesis, Farmington, CT 06030 USA
[2] Univ Connecticut, Ctr Hlth, Dept Pathol, Farmington, CT 06030 USA
[3] Univ Connecticut, Ctr Hlth, Dept Physiol, Farmington, CT 06030 USA
[4] Univ Connecticut, Ctr Hlth, Dept Med, Farmington, CT 06030 USA
[5] Univ Connecticut, Ctr Hlth, Dept Genet & Dev Biol, Farmington, CT 06030 USA
[6] Connecticut Childrens Med Ctr, Div Infect Dis, Hartford, CT 06106 USA
关键词
D O I
10.1128/IAI.70.9.5304-5306.2002
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
A new strain of Babesia micron (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. micron 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 alphabeta (TCRbeta(-/-)) or gamma interferon (IFN-gamma) (IFN-gamma(-/-)) knockout mice following inoculation with the KR-1-strain. SCID mice and TCRalphabeta knockouts sustained a severe but nonlethal parasitemia averaging 35 to 45% infected erythrocytes. IFN-gamma-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-gamma.
引用
收藏
页码:5304 / 5306
页数:3
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