Current understanding of immunity to Trypanosoma cruzi infection and pathogenesis of Chagas disease

Fabiana S. Machado, Walderez O. Dutra, Lisia Esper, Kenneth J. Gollob, Mauro M. Teixeira, Stephen M. Factor, Louis M. Weiss, Fnu Nagajyothi, Herbert B. Tanowitz, Nisha J. Garg

Research output: Contribution to journalReview articlepeer-review

164 Scopus citations


Chagas disease caused by Trypanosoma cruzi remains an important neglected tropical disease and a cause of significant morbidity and mortality. No longer confined to endemic areas of Latin America, it is now found in non-endemic areas due to immigration. The parasite may persist in any tissue, but in recent years, there has been increased recognition of adipose tissue both as an early target of infection and a reservoir of chronic infection. The major complications of this disease are cardiomyopathy and megasyndromes involving the gastrointestinal tract. The pathogenesis of Chagas disease is complex and multifactorial involving many interactive pathways. The significance of innate immunity, including the contributions of cytokines, chemokines, reactive oxygen species, and oxidative stress, has been emphasized. The role of the components of the eicosanoid pathway such as thromboxane A2 and the lipoxins has been demonstrated to have profound effects as both pro- and anti-inflammatory factors. Additionally, we discuss the vasoconstrictive actions of thromboxane A2 and endothelin-1 in Chagas disease. Human immunity to T. cruzi infection and its role in pathogen control and disease progression have not been fully investigated. However, recently, it was demonstrated that a reduction in the anti-inflammatory cytokine IL-10 was associated with clinically significant chronic chagasic cardiomyopathy.

Original languageEnglish (US)
Pages (from-to)753-770
Number of pages18
JournalSeminars in Immunopathology
Issue number6
StatePublished - Nov 2012

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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