Evasion of immune responses by Trypanosoma cruzi, the etiological agent of Chagas disease.
Infection with the protozoan parasite Trypanosoma cruzi leads to Chagas disease, which affects millions of people in Latin America. Infection with T. cruzi cannot be eliminated by the immune system. A better understanding of immune evasion mechanisms is required in order to develop more effective vaccines. During the acute phase, parasites replicate extensively and release immunomodulatory molecules that delay parasite-specific responses mediated by T cells. This immune evasion allows the parasite to spread in the host. In the chronic phase, parasite evasion relies on its replication strategy of hijacking the TGF-β signaling pathway involved in inflammation and tissue regeneration. In this article, the mechanisms of immune evasion described for T. cruzi are reviewed.
Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil. gdosreis@biof.ufrj.br
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DosReis
D000208:Acute Disease; D000953:Antigens, Protozoan / Q000276:immunology; D014355:Chagas Disease / Q000276:immunology* / Q000469:parasitology; D002908:Chronic Disease; D006790:Host-Parasite Interactions / Q000276:immunology; D006801:Humans; D057131:Immune Evasion / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000276:immunology*; D014349:Trypanosoma cruzi / Q000276:immunology*
D000953:Antigens, Protozoan; D016212:Transforming Growth Factor beta