A point mutation in the Ncr1 signal peptide impairs the development of innate lymphoid cell subsets.

ABSTRACT: NKp46 (CD335) is a surface receptor shared by both human and mouse natural killer (NK) cells and innate lymphoid cells (ILCs) that transduces activating signals necessary to eliminate virus-infected cells and tumors. Here, we describe a spontaneous point mutation of cysteine to arginine (C14R) in the signal peptide of the NKp46 protein in congenic Ly5.1 mice and the newly generated NCR^B6C14R strain. Ly5.1^C14R NK cells expressed similar levels of Ncr1 mRNA as C57BL/6, but showed impaired surface NKp46 and reduced ability to control melanoma tumors in vivo. Expression of the mutant NKp46^C14R in 293T cells showed that NKp46 protein trafficking to the cell surface was compromised. Although Ly5.1^C14R mice had normal number of NK cells, t

SUBMITTER: Almeida FF 

PROVIDER: S-EPMC6169588 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature