Immunology, Transplantation and Infectious diseases

Autoimmunity and vascular inflammation


Group leader

Angelo Manfredi


Inflammation is a homeostatic process triggered by microbial components and tissue damage. The cellular components that reach the extracellular environment as a consequence of cellular stress and death or activation are recognized by leukocytes which in turn determine the eventual outcome of the process in terms of tissue regeneration and repair or on the other handof inflammatory damage that becomes chronic and self- suffcient, causing tissue remodeling and loss of function. Process abnormalities, particularly in the phagocytic clearance of dead cells, debris, activated platelets, microparticles play a key role in autoimmune diseases.

These alterations contribute to the origin of autoimmunity and to the amplification and acceleration of the clinical features that determine the specific characteristics of each disease. Persistent vascular inflammation, in particular, reflects a vicious circle through which in ammatory leukocytes are attracted and activated in the walls of vessels that further damage. Restoring the regulatory network of signals connecting leukocytes, platelets and endothelial cells could be useful to limit the harmful consequences of the process.

Research activity

The group is particularly interested in the identification of molecular mechanisms that lead to the perpetuation of the inflammatory response and autoimmunity, with particular attention to the role of endogenous adjuvants released after necrosis (Pattern Molecular Damage-Associated, DAMPS, or Alarmins) and humoral innate immunity.