Trypanosoma cruzi immune evasion mediated by host cell-derived microvesicles

Igor Cestari, Ephraim Ansa-Addo, Poliana Deolindo, Jameel M Inal, Marcel I Ramirez

Research output: Contribution to journalArticlepeer-review

97 Citations (Scopus)


The innate immune system is the first mechanism of vertebrate defense against pathogen infection. In this study, we present evidence for a novel immune evasion mechanism of Trypanosoma cruzi, mediated by host cell plasma membrane-derived vesicles. We found that T. cruzi metacyclic trypomastigotes induced microvesicle release from blood cells early in infection. Upon their release, microvesicles formed a complex on the T. cruzi surface with the complement C3 convertase, leading to its stabilization and inhibition, and ultimately resulting in increased parasite survival. Furthermore, we found that TGF-β-bearing microvesicles released from monocytes and lymphocytes promoted rapid cell invasion by T. cruzi, which also contributed to parasites escaping the complement attack. In addition, in vivo infection with T. cruzi showed a rapid increase of microvesicle levels in mouse plasma, and infection with exogenous microvesicles resulted in increased T. cruzi parasitemia. Altogether, these data support a role for microvesicles contributing to T. cruzi evasion of innate immunity.

Original languageEnglish
Pages (from-to)1942-52
Number of pages11
JournalJournal of Immunology
Issue number4
Publication statusPublished - 15 Feb 2012


  • Animals
  • Cell Membrane
  • Cells, Cultured
  • Chagas Disease
  • Complement C3-C5 Convertases
  • Cytoplasmic Vesicles
  • Erythrocytes
  • Host-Pathogen Interactions
  • Humans
  • Immune Evasion
  • Immunity, Innate
  • Lymphocytes
  • Mice
  • Mice, Inbred BALB C
  • Monocytes
  • Transforming Growth Factor beta
  • Trypanosoma cruzi
  • Journal Article
  • Research Support, Non-U.S. Gov't


Dive into the research topics of 'Trypanosoma cruzi immune evasion mediated by host cell-derived microvesicles'. Together they form a unique fingerprint.

Cite this