The long pentraxin PTX3: A prototypical sensor of tissue injury and a regulator of homeostasis

Abstract

Tissue damage frequently occurs. The immune system senses it and enforces homeostatic responses that lead to regeneration and repair. The synthesis of acute phase molecules is emerging as a crucial event in this program. The prototypic long pentraxin PTX3 orchestrates the recruitment of leukocytes, stabilizes the provisional matrix in order to facilitate leukocyte and stem progenitor cells trafficking, promotes swift and safe clearance of dying cells and of autoantigens, limiting autoimmunity and protecting the vasculature. These non-redundant actions of PTX3 are necessary for the resolution of inflammation. Recent studies have highlighted the mechanisms by which PTX3 adapts the functions of innate immune cells, orchestrates tissue repair and contributes to select the appropriate acquired immune response in various tissues. Conversely, PTX3 continues to be produced in diseases where the inflammatory response does not resolve. It is therefore a valuable biomarker for more precise and personalized stratification of patients, often independently predicting clinical evolution and outcome. There is strong promise for novel therapies based on understanding the mechanisms with which PTX3 plays its homeostatic role, especially in regulating leukocyte migration and the resolution of inflammatory processes.

Pentraxin-3 is not related to disease severity in cirrhosis and hepatocellular carcinoma patients

“…Impaired hepatocyte function and accordingly CRP synthesis limit the diagnostic value of CRP in patients with decompensated liver cirrhosis [8]. PTX3 is a reliable marker for the activation of immune cells and was supposed to be superior to CRP in these patients [9].…”

Bariatric surgery results in restoration of physiological plasma levels of pentraxine‑3

“…PTX3 deficient animals had higher deposition of C3 (complement system) in the damaged tissue, thus it is possible that the protective function of PTX3 may transpire through prevention of tissue damage by excessive complement deposition (13). PTX3 inhibits activation of the classic complement pathway by preventing an interaction between immunoglobulins and C1q (14), and inhibits the alternate pathway by controlling the deposition of H factor in apoptotic cells (15).…”

Pentraxin 3 and its role in tissue repair

“…W mysich modelach niezakaźnego uszkodzenia tkanki, niedobór długiej pentraksyny związany był ze zmienioną odpowiedzią zakrzepową, zwiększonym odkładaniem fibryny, po którym następowało zwiększone odkładanie się kolagenu [8,18,23,24]. Na skutek uszkodzenia tkanki następowało indukowanie miejscowego wydzielania PTX3.…”