Antidesmoglein Autoantibodies in Silicosis Patients with No Bullous Diseases

Abstract

Background: Pemphigus is an autoimmune bullous disease characterized by the presence of antidesmoglein autoantibodies. However, the mechanism of its autoantibody production remains unknown. In previous reports, we have described rare cases of pemphigus and pemphigoid associated with silicosis. It is well known that during long-term silicosis, some autoimmune diseases, such as systemic sclerosis, systemic lupus erythematosus or rheumatoid arthritis, can occur. Objective: The aim of this study was to explore the presence of pemphigus or pemphigoid autoantibodies in silicosis patients without clinical bullous diseases or collagen diseases. Method: The presence of pemphigus antibodies was examined in 54 silicosis patients with no associated bullous diseases, using immunofluorescence, the enzyme-linked immunosorbent assay (ELISA) for desmoglein 1 and 3, and immunoblotting methods. In the antibody-positive cases, HLA genotyping of peripheral lymphocytes was performed with PCR-RFLP. Results: Seven out of the 54 patients were found to be positive for pemphigus antibodies and 1 for bullous pemphigoid by immunofluorescence. In addition, by ELISA, 6 patients were found to be positive against the desmoglein 1 antigen, 2 against the desmoglein 3 antigen and 2 against both desmoglein 1 and desmoglein 3. Conclusion: The results of the present study strongly suggest the occurrence of pemphigus and pemphigoid autoantibodies in patients with silicosis. It remains unclear whether such patients will develop an autoimmune bullous disease in the future. Accordingly, long-term follow-up of antibody-positive patients is required.

Involvement of IL-10 and Bcl-2 in resistance against an asbestos-induced apoptosis of T cells

“…We have been investigating the immunological features of patients with silicosis and previously found an aberrant [31][32][33][34][35][36]. In addition, we have reported the experimental effects of asbestos, mainly chrysotile, on human immune-competent cells and demonstrated that T cells exposed to chrysotile undergo apoptosis via death-receptor and mitochondrial pathways [15,18].…”

Silica exposure and altered regulation of autoimmunity

“…We also reported silicosis patients who were positive for anti-desmoglein autoantibody, and these patients were usually positive if possessing pemphigus vulgaris but without any symptoms of bullous diseases [36].…”

Induction of CD69 antigen expression in peripheral blood mononuclear cells on exposure to silica, but not by asbestos/chrysotile-A

“…In addition, a small number of silicosis patients developed 0165 immunological diseases without presenting with respiratory disorders after exposure to silica compounds [19]. In addition, many autoantibodies are found in these patients [20][21][22][23][24].…”