Abstract
In the literature there are no clinical and morphological data that would prove the participation of hypersensitivity reactions, autoimmune and immunocomplex processes in the development of granulomatosis in the arteries in atherosclerosis. In cholesterol mature macrophage granulomas (plaques), markers of immune inflammation are not detected - epithelioid and giant multinuclear Pirogov-Langhans cells; in xanthogranulomas there are giant multinucleated cells of foreign bodies. Granulomatosis in the arteries is induced by endogenous foreign bodies – lipid foci containing non-antigenic, non-hydrolysable cholesterol by macrophage lysosomal enzymes. The properties of its molecule, crystallization and insolubility in the blood and interstitial fluid are the cause of the unresolved nature of the developing inflammation in the arteries.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
