Evolution of the Ly49 and Nkrp1 recognition systems

被引：85

作者：

Carlyle, James R. ^{[1
,2
]}

Mesci, Aruz ^{[1
,2
]}

Fine, Jason H. ^{[1
,2
]}

Chen, Peter ^{[1
,2
]}

Belanger, Simon ^{[3
]}

Tai, Lee-Hwa ^{[3
]}

Makrigiannis, Andrew P. ^{[3
]}

机构：

[1] Univ Toronto, Dept Immunol, Toronto, ON M4N 3M5, Canada

[2] Sunnybrook Res Inst, Toronto, ON M4N 3M5, Canada

[3] Univ Montreal, Inst Rech Clin Montreal, Lab Mol Immunol, Montreal, PQ H2W 1R7, Canada

来源：

SEMINARS IN IMMUNOLOGY | 2008年 / 20卷 / 06期

基金：

加拿大自然科学与工程研究理事会; 加拿大健康研究院;

关键词：

Ly49; Nkrp1; Clr/Ocil; Natural killer cell;

D O I：

10.1016/j.smim.2008.05.004

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 [免疫学];

摘要：

The Ly49 and Nkrp1 loci encode structurally and functionally related cell surface proteins that positively or negatively regulate natural killer (NK) cell-mediated cytotoxicity and cytokine production. Yet despite their clear relatedness and genetic linkage within the NK gene complex (NKC), these two multi-gene families have adopted dissimilar evolutionary strategies. The Ly49 genes are extremely polymorphic and evolutionarily dynamic, with distinct gene numbers, remarkable allelic diversity, and varying MHC-I-ligand specificities and affinities among different murine haplotypes. In contrast, the Nkrp1 genes have opted for overall conservation of genomic organization, sequences, and ligand specificities, with only limited and focused allelic polymorphism. Possible selection pressures driving such varied evolution of the two gene families may include disequilibrium from ligand co-inheritance, pathogen immunoevasin strategies, flexibility in host counter-evolution mechanisms, and the prevalence and dynamics of inherent repetitive elements. (C) 2008 Elsevier Ltd. All rights reserved.

引用

页码：321 / 330

页数：10

共 90 条

[1]

Cmv4, a new locus linked to the NK cell gene complex, controls innate resistance to cytomegalovirus in wild-derived mice [J].