Genetic Polymorphism of KIR2DL4 (CD158d), a Putative NK Cell Receptor for HLA-G, Does Not Influence Susceptibility to Asthma

Human leukocyte antigen (HLA)-G is upregulated on the bronchial epithelium of asthma patients and genetic polymorphism affecting expression of HLA-G has been reported to influence susceptibility to asthma. As the NK cell receptor KIR2DL4 has been reported to induce interferon gamma (IFNy) secretion...

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Main Authors: Le Page, M., Goodridge, J., Zhang, Guicheng, Holt, P., Sly, P., Witt, C.
Format: Journal Article
Published: Blackwell Munksgaard 2013
Subjects:
Online Access:http://hdl.handle.net/20.500.11937/43670
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author Le Page, M.
Goodridge, J.
Zhang, Guicheng
Holt, P.
Sly, P.
Witt, C.
author_facet Le Page, M.
Goodridge, J.
Zhang, Guicheng
Holt, P.
Sly, P.
Witt, C.
author_sort Le Page, M.
building Curtin Institutional Repository
collection Online Access
description Human leukocyte antigen (HLA)-G is upregulated on the bronchial epithelium of asthma patients and genetic polymorphism affecting expression of HLA-G has been reported to influence susceptibility to asthma. As the NK cell receptor KIR2DL4 has been reported to induce interferon gamma (IFNy) secretion when ligated with HLA-G, we postulated that the 9A/10A genetic polymorphism of KIR2DL4 which influences receptor structure may influence susceptibility to asthma. KIR2DL4 genotypes weredetermined in two cohorts of children (n=219 and n=1356) in whom total serum IgE, allergen-specific IgE, atopy, bronchial reactivity and asthma symptoms had been studied between birth and 14 years. No reproducible associations with KIR2DL4 genotype were identified, leading us to conclude that the KIR2DL4 9A/10A polymorphism has no influence on susceptibility to asthma.
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institution Curtin University Malaysia
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spelling curtin-20.500.11937-436702017-09-13T13:39:38Z Genetic Polymorphism of KIR2DL4 (CD158d), a Putative NK Cell Receptor for HLA-G, Does Not Influence Susceptibility to Asthma Le Page, M. Goodridge, J. Zhang, Guicheng Holt, P. Sly, P. Witt, C. atopy asthma KIR2DL4 CD158d Human leukocyte antigen (HLA)-G is upregulated on the bronchial epithelium of asthma patients and genetic polymorphism affecting expression of HLA-G has been reported to influence susceptibility to asthma. As the NK cell receptor KIR2DL4 has been reported to induce interferon gamma (IFNy) secretion when ligated with HLA-G, we postulated that the 9A/10A genetic polymorphism of KIR2DL4 which influences receptor structure may influence susceptibility to asthma. KIR2DL4 genotypes weredetermined in two cohorts of children (n=219 and n=1356) in whom total serum IgE, allergen-specific IgE, atopy, bronchial reactivity and asthma symptoms had been studied between birth and 14 years. No reproducible associations with KIR2DL4 genotype were identified, leading us to conclude that the KIR2DL4 9A/10A polymorphism has no influence on susceptibility to asthma. 2013 Journal Article http://hdl.handle.net/20.500.11937/43670 10.1111/tan.12185 Blackwell Munksgaard restricted
spellingShingle atopy
asthma
KIR2DL4
CD158d
Le Page, M.
Goodridge, J.
Zhang, Guicheng
Holt, P.
Sly, P.
Witt, C.
Genetic Polymorphism of KIR2DL4 (CD158d), a Putative NK Cell Receptor for HLA-G, Does Not Influence Susceptibility to Asthma
title Genetic Polymorphism of KIR2DL4 (CD158d), a Putative NK Cell Receptor for HLA-G, Does Not Influence Susceptibility to Asthma
title_full Genetic Polymorphism of KIR2DL4 (CD158d), a Putative NK Cell Receptor for HLA-G, Does Not Influence Susceptibility to Asthma
title_fullStr Genetic Polymorphism of KIR2DL4 (CD158d), a Putative NK Cell Receptor for HLA-G, Does Not Influence Susceptibility to Asthma
title_full_unstemmed Genetic Polymorphism of KIR2DL4 (CD158d), a Putative NK Cell Receptor for HLA-G, Does Not Influence Susceptibility to Asthma
title_short Genetic Polymorphism of KIR2DL4 (CD158d), a Putative NK Cell Receptor for HLA-G, Does Not Influence Susceptibility to Asthma
title_sort genetic polymorphism of kir2dl4 (cd158d), a putative nk cell receptor for hla-g, does not influence susceptibility to asthma
topic atopy
asthma
KIR2DL4
CD158d
url http://hdl.handle.net/20.500.11937/43670