Abstract

Trypanosoma cruzi is the causative agent of Chagas’ disease, a chronic illness affecting 10 million people around the world. The complement system plays an important role during microbial infection of mammalian hosts. Complement lectin pathway recognition molecules, mannose-binding lectin (MBL), ficolins and CL-11, bind to specific carbohydrates on pathogens, triggering complement activation through MBL-associated serine protease-2 (MASP-2). Previous in vitro work showed that human MBL and ficolins contribute to T. cruzi lysis. However, MBL-deficient mice are only moderately compromised in their defense against the parasite, as they may still activate the lectin pathway through ficolins and CL-11. Here we assessed MASP-2-deficient mice, the only presently available mouse line with total lectin pathway deficiency, for a phenotype in T. cruzi infection. Total absence of complement lectin pathway activity did not confer higher susceptibility to T. cruzi infection, suggesting that it plays a minor role in the immune response against the parasite.