Evolution of the Ly49 and Nkrp1 recognition systems

James R. Carlyle; Aruz Mesci; Jason H. Fine; Peter Chen; Simon Bélanger; Lee Hwa Tai; Andrew P. Makrigiannis

doi:10.1016/j.smim.2008.05.004

Evolution of the Ly49 and Nkrp1 recognition systems

James R. Carlyle, Aruz Mesci, Jason H. Fine, Peter Chen, Simon Bélanger, Lee Hwa Tai, Andrew P. Makrigiannis

Producción científica: Contribución a una revista › Artículo de revisión › revisión exhaustiva

90 Citas (Scopus)

Resumen

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.

Idioma original	English
Páginas (desde-hasta)	321-330
Número de páginas	10
Publicación	Seminars in Immunology
Volumen	20
N.º	6
DOI	https://doi.org/10.1016/j.smim.2008.05.004
Estado	Published - dic. 2008
Publicado de forma externa	Sí

Nota bibliográfica

Funding Information:
This work was supported by grants from the Canadian Institutes of Health Research (CIHR; FRN 74754 to J.R.C.; FRN 62841 to A.P.M.; and FRN 86630 to J.R.C. and A.P.M.). J.R.C. was supported by a Career Development Award from the International Human Frontier Science Program Organization, and currently holds an Early Researcher Award from the Ontario Ministry of Research and Innovation, a New Investigator Award from the CIHR, and an Investigators in the Pathogenesis of Infectious Disease Award from the Burroughs Wellcome Fund. A.P.M. is supported by a New Investigator Award from the CIHR and a Junior Level-2 Fonds de la recherche en santé du Québec (FRSQ) Award. A.M. was supported by an Ontario Graduate Scholarship (OGS) Award; J.H.F. is supported by a Doctoral Post-Graduate Scholarship from the Natural Sciences and Engineering Research Council (NSERC); P.C. is supported by an OGS Award; S.B. is supported by a scholarship from the FRSQ. L-H.T. is supported by a CIHR Cancer Training Program scholarship.

ASJC Scopus Subject Areas

Immunology and Allergy
Immunology

PubMed: MeSH publication types

Journal Article
Research Support, Non-U.S. Gov't
Review

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title = "Evolution of the Ly49 and Nkrp1 recognition systems",

abstract = "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.",

author = "Carlyle, {James R.} and Aruz Mesci and Fine, {Jason H.} and Peter Chen and Simon B{\'e}langer and Tai, {Lee Hwa} and Makrigiannis, {Andrew P.}",

note = "Funding Information: This work was supported by grants from the Canadian Institutes of Health Research (CIHR; FRN 74754 to J.R.C.; FRN 62841 to A.P.M.; and FRN 86630 to J.R.C. and A.P.M.). J.R.C. was supported by a Career Development Award from the International Human Frontier Science Program Organization, and currently holds an Early Researcher Award from the Ontario Ministry of Research and Innovation, a New Investigator Award from the CIHR, and an Investigators in the Pathogenesis of Infectious Disease Award from the Burroughs Wellcome Fund. A.P.M. is supported by a New Investigator Award from the CIHR and a Junior Level-2 Fonds de la recherche en sant{\'e} du Qu{\'e}bec (FRSQ) Award. A.M. was supported by an Ontario Graduate Scholarship (OGS) Award; J.H.F. is supported by a Doctoral Post-Graduate Scholarship from the Natural Sciences and Engineering Research Council (NSERC); P.C. is supported by an OGS Award; S.B. is supported by a scholarship from the FRSQ. L-H.T. is supported by a CIHR Cancer Training Program scholarship.",

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AU - Carlyle, James R.

AU - Mesci, Aruz

AU - Fine, Jason H.

AU - Chen, Peter

AU - Bélanger, Simon

AU - Tai, Lee Hwa

AU - Makrigiannis, Andrew P.

N1 - Funding Information: This work was supported by grants from the Canadian Institutes of Health Research (CIHR; FRN 74754 to J.R.C.; FRN 62841 to A.P.M.; and FRN 86630 to J.R.C. and A.P.M.). J.R.C. was supported by a Career Development Award from the International Human Frontier Science Program Organization, and currently holds an Early Researcher Award from the Ontario Ministry of Research and Innovation, a New Investigator Award from the CIHR, and an Investigators in the Pathogenesis of Infectious Disease Award from the Burroughs Wellcome Fund. A.P.M. is supported by a New Investigator Award from the CIHR and a Junior Level-2 Fonds de la recherche en santé du Québec (FRSQ) Award. A.M. was supported by an Ontario Graduate Scholarship (OGS) Award; J.H.F. is supported by a Doctoral Post-Graduate Scholarship from the Natural Sciences and Engineering Research Council (NSERC); P.C. is supported by an OGS Award; S.B. is supported by a scholarship from the FRSQ. L-H.T. is supported by a CIHR Cancer Training Program scholarship.

PY - 2008/12

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N2 - 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.

AB - 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.

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Evolution of the Ly49 and Nkrp1 recognition systems

Resumen

Nota bibliográfica

ASJC Scopus Subject Areas

PubMed: MeSH publication types

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