Cellular Sensitivity to Collagen in Thromboangiitis Obliterans

Abstract

We studied 39 patients with thromboangiitis obliterans to determine their cellular and humoral immune responses to native human collagen Type I and Type III, which are constituents of blood vessels. Cell-mediated sensitivity to these collagens was measured by an antigen-sensitive thymidine-incorporation assay. The mean stimulation index--the ratio of thymidine incorporation in the presence of antigen to that in its absence--with both Type I and Type III collagens used as antigens was significantly higher in patients with thromboangiitis obliterans than in patients with arteriosclerosis obliterans or in healthy male controls. Lymphocytes from 77 per cent of the patients with thromboangiitis obliterans exhibited cellular sensitivity to human Type I or Type III collagens (or both). Furthermore, in 17 of 39 serum samples from the patients with thromboangiitis obliterans a low but significant level of anticollagen antibody activity was detected, whereas there was no antibody activity in serum samples from controls. These results suggest that there is a distinct etiologic factor in this disease and also raise the possibility of differentiating between thromboangiitis obliterans and arteriosclerosis obliterans by immunologic means.

Buerger's Disease and Secondary Hyperparathyroidism Associated with Chronic Hemodialysis

“…Complete abstinence from tobacco use (including pipe smoking and tobacco chewing) will halt disease progression (5). More recently, investigators have shown that patients with TAO have an increased cellular immune response to collagen types I and III, which are normal constituents of blood vessels (11). This type of autoimmune phenomenon has been supported further by the presence of anticollagen antibodies in some patients with Buerger's disease (11).…”

“…More recently, investigators have shown that patients with TAO have an increased cellular immune response to collagen types I and III, which are normal constituents of blood vessels (11). This type of autoimmune phenomenon has been supported further by the presence of anticollagen antibodies in some patients with Buerger's disease (11). Furthermore, certain human leukocyte antigens (HLA) (types A9, B5, and DR4) have been reported to occur in a greater-than-expected frequency in patients with TAO, suggesting a possible genetic predisposition to this disease (12,13).…”

Thromboangiitis Obliterans (Buerger's Disease)

“…Use or exposure to tobacco plays central role in the initiation and progression of the disease. By using an antigen-sensitive thymidine-incorporation assay, Adar et al [20] showed that patients with TAO have an increased cellular sensitivity to type I and III collagen, compared to that in patients with arteriosclerosis obliterans or healthy males. De Moerloose et al [21] found a marked decrease in frequency of the HLA-B12 antigen in patients with Buerger's disease (2.2% vs. 28% in controls).…”

Targeting novel antigens in the arterial wall in thromboangiitis obliterans.

“…Various studies were undertaken to examine the mechanism of the immune injury. An increased cellular and humoral response to collagen [28,29], circulating immune complexes [30,31], elevated antielastin titers [32] and abnormal elastin degradation [33] were reported. The altered production of IL-6, IL-12 and IL-10, the increased apoptosis as well as the elevated levels of circulating immune complexes were proposed to be the reason for the persisting immune inflammation in TAO [34].…”