Cyclosporin A treatment converts Leishmania donovani-infected C57BL/10 (curing) mice to a noncuring phenotype.
作者信息
Adinolfi L E, Bonventre P F
机构信息
Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati Medical Center, Ohio 45267.
出版信息
Infect Immun. 1990 Sep;58(9):3151-3. doi: 10.1128/iai.58.9.3151-3153.1990.
Abstract
Cyclosporin A prevents visceralization of Leishmania major infection of BALB/c mice (N. C. Behforouz, C. D. Wenger, and B. A. Mathison, J. Immunol. 136:3067-3075, 1986; W. Solbach, K. Forberg, E. Kammerer, C. Bogdan, and M. Rollinghoff, J. Immunol. 134:702-707, 1986). We report that cyclosporin A exacerbates disseminated leishmaniasis caused by L. donovani in C57BL/10 mice. Normal mice challenged with 5 x 10(6) amastigotes intravenously cleared the infection within several months by spontaneous acquisition of cell-mediated immunity. In contrast, cyclosporin A administered daily intraperitoneally at a dose of 1.25 mg per mouse prevented development of curative immunity and converted C57BL/10 (curing) mice to a noncuring phenotype. A rationale for the contrasting effects of cyclosporin A in the two murine models of leishmaniasis is provided.
摘要
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