Divisions

Autoimmunity and vascular inflammation

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Head of Unit

Angelo Manfredi

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Inflammation is a homeostatic process triggered by microbial components and tissue damage. The ways in which the cells die, the cellular constituents reach the extracellular environment and are recognized by the cells of the immune system determine the effects of the inflammatory response in terms of:

  • tissue repair,
  • inflammatory damage that becomes chronic and self-sustaining.

Alterations in the early and late phases of the process, in particular in the phagocytic clearance of dead cells and debris, play a key role in systemic autoimmune diseases, wherein the altered response to these signals plays a role in both disease origin and in the amplification mechanism and acceleration of clinical features determining the specific characteristics of each disease. Persiste vascular inflammation, in particular, reflects a vicious circle through which inflammatory leucocytes are attracted and activate in the walls of the vessels that they further damage. Restoration of the regulatory network of signals that connect leucocytes, platelets and endothelial cells might be valuable to limit the noxious 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 Alarmine) and humoral innate immunity.