PubMed1988
The histogenesis of the Aschoff body of rheumatic carditis is controversial. Proliferative Aschoff bodies in heart sections from 6 patients with acute rheumatic heart disease were tested by avidin-biotin peroxidase labeling methods for the presence of desmin, muscle-specific actin, S-100, neurofilament, leukocyte common antigen, receptor for Ulex europeus I lectin, Factor VIII-related antigen, vimentin, alpha 1-antichymotrypsin, and myeloid/histiocyte antigen. Lack of Aschoff body labeling for desmin and muscle-specific actin, S-100 and neurofilament, and Ulex europeus I and Factor VIII-related antigen is not consistent with histogenesis from smooth or striated cardiac muscle, nerve or nerve sheath, and lymphatic or vascular endothelium, respectively. Strong labeling of Aschoff body cells for vimentin is evidence for a mesenchymal origin, and labeling for myeloid/histiocyte antigen is consistent with a histiocytic origin. Furthermore, weak, variable labeling of Aschoff body cells for leukocyte common antigen suggests that at least some Aschoff body cells were originally derived from blood-borne monocytes. Both multinucleated Aschoff cells and "owl's eye," Anitschkow cells label identically, suggesting a common origin. Alpha 1-Antichymotrypsin, a widely utilized marker of histiocytes, was unexpectedly negative. Perhaps histiocytes that form Aschoff bodies do not express this lysosomal enzyme. Aschoff bodies appear to be a unique and distinctive form of granuloma.