Cutting Edge: Check Your Mice-A Point Mutation in the Ncr1 Locus Identified in CD45.1 Congenic Mice with Consequences in Mouse Susceptibility to Infection.
Autor: | Jang Y; Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109., Gerbec ZJ; Blood Center of Wisconsin, Milwaukee, WI 53226.; Department of Medicine, Medical College of Wisconsin, Milwaukee, WI 53226.; Department of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, WI 53226.; Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI 53226; and., Won T; Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109., Choi B; Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109., Podsiad A; Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109., B Moore B; Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109.; Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109., Malarkannan S; Blood Center of Wisconsin, Milwaukee, WI 53226.; Department of Medicine, Medical College of Wisconsin, Milwaukee, WI 53226.; Department of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, WI 53226.; Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI 53226; and., Laouar Y; Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109; ylaouar@umich.edu. |
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Jazyk: | angličtina |
Zdroj: | Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2018 Mar 15; Vol. 200 (6), pp. 1982-1987. Date of Electronic Publication: 2018 Feb 09. |
DOI: | 10.4049/jimmunol.1701676 |
Abstrakt: | B6.SJL- Ptprc a Pepc b /Boy (CD45.1) mice have been used in hundreds of congenic competitive transplants, with the presumption that they differ from C57BL/6 mice only at the CD45 locus. In this study, we describe a point mutation in the natural cytotoxicity receptor 1 ( Ncr1 ) locus fortuitously identified in the CD45.1 strain. This point mutation was mapped at the 40th nucleotide of the Ncr1 locus causing a single amino acid mutation from cysteine to arginine at position 14 from the start codon, resulting in loss of NCR1 expression. We found that these mice were more resistant to CMV due to a hyper innate IFN-γ response in the absence of NCR1. In contrast, loss of NCR1 increased susceptibility to influenza virus, a result that is consistent with the role of NCR1 in the recognition of influenza Ag, hemagglutinin. This work sheds light on potential confounding experimental interpretation when this congenic strain is used as a tool for tracking lymphocyte development. (Copyright © 2018 by The American Association of Immunologists, Inc.) |
Databáze: | MEDLINE |
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