Is the Antitumor Property of Trypanosoma cruzi Infection Mediated by Its Calreticulin

摘要: Eight to 10 million people in 21 endemic countries are infected with Trypanosoma cruzi. However, only 30% of those develop symptoms Chagas’ disease, a chronic, neglected tropical disease worldwide. Similar other pathogens, T. cruzi has evolved resist the host immune response. Studies, performed 80 years ago Soviet Union, proposed that infects tumor cells similar capacity displayed for target tissues such as cardiac, aortic or digestive. An antagonistic relationship between infection and cancer development was also proposed, but molecular mechanisms involved have remained largely unknown. Probably, variety molecules is involved. This review focuses on how calreticulin (TcCRT), exteriorized from endoplasmic reticulum, targets first classical complement component C1 negatively regulates Classical Complement activation cascade, promoting parasite infectivity. We propose this C1-dependent TcCRT-mediated virulence critical explain, at least an important part, inhibit development. will discuss TcCRT, by directly interacting venous arterial endothelial cells, inhibits angiogenesis growth. Thus, these TcCRT functions not illustrate interactions defensive strategies, possible co-evolutionary adaptation privilege prolonged interaction its host.