Human leucocyte antigen class II association in idiopathic bronchiectasis, a disease of chronic lung infection, implicates a role for adaptive immunity


R. Boyton, MRC Clinician Scientist, Lung Immunology Group, National Heart and Lung Institute, Sir Alexander Fleming Building, South Kensington Campus, Faculty of Medicine, Imperial College, London SW7 2AZ, UK.


The aetiology of idiopathic bronchiectasis, a lung disease where chronic inflammation and bacterial infection leads to progressive lung damage, is unknown. A possible role for natural killer cells has been highlighted previously. However, a role for adaptive immunity is suggested by the presence of CD4 and CD8 T cells in diseased lung tissue. Evidence of a human leucocyte antigen (HLA) class II disease association would further implicate a role for adaptive immunity. To establish if there is any HLA association, we analysed HLA-A, HLA-B, HLA-DQA1, HLA-DQB1 and HLA-DRB1 alleles in patients with idiopathic bronchiectasis and controls. Genomic DNA from 92 adults with idiopathic bronchiectasis and 101 healthy controls was analysed by polymerase chain reaction with sequence-specific primers. We found an increase in the prevalence of HLA-DRB1*01 DQA1*01/DQB1*05 genes in idiopathic bronchiectasis; that is, the HLA-DR1, DQ5 haplotype (odds ratio 2·19, 95% confidence interval 1·15–4·16, P = 0·0152) compared with control subjects. The association with HLA-DR1, DQ5 implicates a role for CD4 T cells restricted by these molecules in susceptibility to the progressive lung damage seen in this disease. This may operate either through influencing susceptibility to specific pathogens or to self-reactivity and requires further investigation.