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Adoptive transfer of natural killer cell activity in B6D2F1 mice challenged with Salmonella typhimurium.

作者信息

Griggs N D, Smith R A

机构信息

Department of Microbiology and Cell Science, University of Florida, Gainesville 32611.

出版信息

Cell Immunol. 1991 Jun;135(1):88-94. doi: 10.1016/0008-8749(91)90256-b.

DOI:10.1016/0008-8749(91)90256-b
PMID:2018985
Abstract

The purpose of this study was to extend our previous findings as to the role of murine NK cells in host protection to a challenge infection with virulent Salmonella typhimurium SR-11. B6D2F1 mice were depleted of NK cells with anti-asialo GM1 or a monoclonal antibody, anti-NK 1.1, followed by a salmonellae challenge. Significantly decreased numbers of splenic bacteria (P less than 0.005) in the NK cell-depleted mice were note at 12, 24, and 48 hr postchallenging, compared to the sham-injected control animals. When Percoll gradient-enriched large granular lymphocytes (NK cells) were adoptively transferred to NK cell-depleted mice followed by challenging, the splenic bacterial numbers were comparable to those present in NK cell-intact, control mice. These data indicate that large granular lymphocytes (NK cells) are responsible for the down-regulation of the protective host response in mice challenged with the facultative intracellular parasite. S. typhimurium.

摘要

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N-ethyl-N-nitrosourea-induced mutation in ubiquitin-specific peptidase 18 causes hyperactivation of IFN-αß signaling and suppresses STAT4-induced IFN-γ production, resulting in increased susceptibility to Salmonella typhimurium.
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