This study is a continuation of our previous work that showed that patients with
thromboangiitis obliterans (
TAO;
Buerger's disease) demonstrate a cell-mediated immune response to human artery type-specific
collagens. To investigate the role of cigarette smoking in patients with
TAO, cellular and humoral sensitivity was tested to a tobacco
glycoprotein (TGP)
antigen in 13 patients with
Buerger's disease, 16 healthy smokers, and 12 nonsmoking healthy young male subjects. In this study, patients with
Buerger's disease and healthy smokers had the same rate of cellular response to TGP, whereas nonsmokers did not respond. All three groups had a 30% to 40% measurable antibody response to TGP. If TGP has an immunologic role in the pathogenesis of
TAO, an additional factor (or factors) may be operative. A specific genetic makeup may be one such factor, although at this stage other pathogenic mechanisms cannot be ruled out. Eleven patients with
Buerger's disease and two control groups of 10 young healthy smoking male subjects and 12 young nonsmokers underwent histocompatibility leukocyte
antigen (HLA) typing. Patients with
Buerger's disease had a statistically significantly higher frequency of
HLA-DR4 and a significantly lower frequency of the HLA-DRW6
antigen than had both control groups. Because similar findings have been reported in other
autoimmune diseases, this observation may serve as further evidence that an autoimmune mechanism is involved in
Buerger's disease.