Trypanosoma cruzi Calreticulin: Immune Evasion, Infectivity, and Tumorigenesis

Trends Parasitol. 2020 Apr;36(4):368-381. doi: 10.1016/j.pt.2020.01.007. Epub 2020 Feb 24.

Abstract

To successfully infect, Trypanosoma cruzi evades and modulates the host immune response. T. cruzi calreticulin (TcCalr) is a multifunctional, endoplasmic reticulum (ER)-resident chaperone that, translocated to the external microenvironment, mediates crucial host-parasite interactions. TcCalr binds and inactivates C1 and mannose-binding lectin (MBL)/ficolins, important pattern- recognition receptors (PRRs) of the complement system. Using an apoptotic mimicry strategy, the C1-TcCalr association facilitates the infection of target cells. T. cruzi infection also seems to confer protection against tumorigenesis. Thus, recombinant TcCalr has important antiangiogenic properties, detected in vitro, ex vivo, and in ovum, most likely contributing at least in part, to its antitumor properties. Consequently, TcCalr is useful for investigating key issues of host-parasite interactions and possible new immunological/pharmacological interventions in the areas of Chagas' disease and experimental cancer.

Keywords: Trypanosoma cruzi; calreticulin; complement; infectivity; tumorigenesis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Calreticulin / immunology*
  • Carcinogenesis / immunology*
  • Chagas Disease / complications*
  • Chagas Disease / immunology*
  • Chagas Disease / parasitology
  • Chagas Disease / pathology
  • Host-Parasite Interactions / immunology*
  • Humans
  • Immune Evasion / immunology
  • Neoplasms / etiology*
  • Neoplasms / immunology
  • Trypanosoma cruzi / pathogenicity*
  • Trypanosoma cruzi / physiology
  • Virulence Factors / immunology

Substances

  • Calreticulin
  • Virulence Factors