Many diseases, notably those having a strong autoimmune component, have been shown to have an association with specific
human leukocyte antigens (HLA). The molecular basis for this genetic association with disease is the fact that HLA bind and present
peptides derived from self and foreign
protein antigens to the immune system for recognition and activation of the immune response. Previous studies with heterogeneous groups of
alopecia areata (AA) patients have suggested associations with some HLA class I and
class II antigens. For this study we selected only patients with long-standing disease and stratified them into two groups by strict definitions of duration and extent of disease: those with patchy AA and those with either
alopecia totalis (AT) or
alopecia universalis (AU). The patients were tissue typed for HLA
class II antigens by biomolecular methods that provided
antigen discrimination at an allele level. More than 80% of all of the AA patients typed were positive for the
antigen DQB1*03 (DQ3), suggesting that this
antigen is a marker for general susceptibility to AA. In addition, two other
antigens were found significantly increased in frequency only in the group of AT/AU patients, DRB1*0401 (DR4) and DQB1*0301(DQ7). This strongly suggests that the two clinical types of AA, namely patchy AA versus AT/AU, can be distinguished by a genetically based predisposition to extent of disease.