期刊
JOURNAL OF IMMUNOLOGY
卷 200, 期 6, 页码 1982-1987出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1701676
关键词
-
类别
资金
- National Institutes of Health [R01 AI102893, R01 CA179363, R01 HL119682, R01 AI083642]
- Midwest Athletes Against Childhood Cancer Fund
- Gardetto Family Foundation
- Nicholas Family Foundation
- American Association of Immunologists Careers in Immunology Grant [N023607]
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-gamma 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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据