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.