Lack of association of human leukocyte antigen-B7 with COPD and rate of decline in lung function

Ikuma Kasuga, Jian Ruan, John E. Connett, Nicholas R. Anthonisen, Andrew J. Sandford

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

Background: Although variation in the human leukocyte antigen (HLA) locus is associated with various diseases, there have been a limited number of studies that have examined the possible role of HLA in chronic obstructive pulmonary disease (COPD). Only HLA-B7 has been shown to be correlated with low forced expiratory volume in 1 s (FEV1) in Caucasians; however, this finding has not been replicated. The aim of this study was to investigate the contribution of the HLA-B7 allele to COPD and to rate of decline of lung function. Methods: We determined the prevalence of HLA-B7 in a group of COPD patients and a non-obstructed control group of smokers by using a polymerase chain reaction-based genotyping assay. We also determined the prevalence of HLA-B7 in smokers selected from the National Heart Lung and Blood Institute, Lung Health Study for having the fastest and slowest decline of lung function. Results: No significant difference was found in the frequency of HLA-B7 between the COPD and non-obstructed groups. There was also no significant association of HLA-B7 with rate of decline of lung function. Conclusion: These data indicate that HLA-B7 does not contribute to COPD or rate of decline of FEV1 in smokers.

Original languageEnglish (US)
Pages (from-to)1528-1533
Number of pages6
JournalRespiratory Medicine
Volume99
Issue number12
DOIs
StatePublished - Dec 2005

Bibliographical note

Funding Information:
This work was supported by National Heart, Lung, and Blood Institute Grant 1R01HL066569-01. The Lung Health Study was also supported by contract N01-HR-46002 from the Division of Lung Diseases of the National Heart, Lung and Blood Institute (NHLBI). The authors gratefully acknowledge the NHLBI for the recruitment and characterization of this study. Andrew Sandford is a recipient of a Canada Research Chair. The authors would like to express their gratitude to Helen Voelker for assistance with the statistical analyses and Drs. Peter Paré and James Hogg for critical review of the manuscript.

Keywords

  • COPD
  • HLA
  • Lung function

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