HLX1 gene variants influence the development of childhood asthma

J Allergy Clin Immunol. 2009 Jan;123(1):82-88.e6. doi: 10.1016/j.jaci.2008.09.047. Epub 2008 Nov 28.

Abstract

Background: Major transcription factors controlling T(H)1 and T(H)2 development, such as T-box transcription factor and GATA3, might be centrally involved in asthma and atopic diseases. Only recently, the homeobox transcription factor H.20-like homeobox 1 (HLX1), interacting closely with T-box transcription factor, has been identified as an important regulator of T(H)1 differentiation and suppressor of T(H)2 commitment.

Objective: We investigated whether genetic variations in the HLX1 gene exist and whether these could affect the development of childhood asthma.

Methods: The HLX1 gene was resequenced in 80 chromosomes. Associations between identified polymorphisms, asthma, and atopic diseases were investigated in German children (total n = 3099) from the cross-sectional International Study of Asthma and Allergy in Childhood phase II. Functional properties of polymorphisms were studied by using luciferase reporter gene assays and electrophoretic mobility shift assays in T cells. All statistical analyses were performed with SAS/Genetics software (SAS Institute, Inc, Cary, NC).

Results: Nineteen polymorphisms were identified in the HLX1 gene, and 2 tagging single nucleotide polymorphisms representing 7 polymorphisms were associated with childhood asthma in our study population. Two promoter polymorphisms, C-1407T and C-742G, contained in 1 tagging block were associated with asthma (odds ratio, 1.44; 95% CI, 1.11-1.86; P = .0061), significantly decrease promoter transactivation, and disrupt specificity protein-transcription factor binding in in vitro experiments.

Conclusions: Our data suggest that polymorphisms in the HLX1 gene increase the risk for childhood asthma. On the cellular level, altered binding of specificity protein-transcription factors to the HLX1 promoter and subsequent changes in HLX1 gene expression might contribute to these effects.

Publication types

  • Multicenter Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Asthma / genetics*
  • Asthma / immunology
  • Asthma / metabolism
  • Child
  • Cross-Sectional Studies
  • Female
  • GATA3 Transcription Factor / genetics
  • GATA3 Transcription Factor / immunology
  • GATA3 Transcription Factor / metabolism
  • Homeodomain Proteins / genetics*
  • Homeodomain Proteins / immunology
  • Homeodomain Proteins / metabolism
  • Humans
  • Male
  • Polymorphism, Single Nucleotide*
  • Promoter Regions, Genetic / genetics*
  • Promoter Regions, Genetic / immunology
  • Risk Factors
  • Th1 Cells / immunology
  • Th1 Cells / metabolism
  • Th2 Cells / immunology
  • Th2 Cells / metabolism
  • Transcription Factors / genetics*
  • Transcription Factors / immunology
  • Transcription Factors / metabolism

Substances

  • GATA3 Transcription Factor
  • GATA3 protein, human
  • HLX protein, human
  • Homeodomain Proteins
  • Transcription Factors