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Journal of Immunology Research - Volume 2015 2015, Article ID 178947, 7 pages -

Review Article

Instituto de Microbiologia, Universidade Federal do Rio de Janeiro, 21.941-590 Rio de Janeiro, RJ, Brazil

Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, 21.941-590 Rio de Janeiro, RJ, Brazil

Received 24 November 2014; Accepted 31 December 2014

Academic Editor: Oguz Kul

Copyright © 2015 Ana Flávia Nardy et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Microbes have evolved a diverse range of strategies to subvert the host immune system. The protozoan parasite Trypanosoma cruzi, the causative agent of Chagas disease, provides a good example of such adaptations. This parasite targets a broad spectrum of host tissues including both peripheral and central lymphoid tissues. Rapid colonization of the host gives rise to a systemic acute response which the parasite must overcome. The parasite in fact undermines both innate and adaptive immunity. It interferes with the antigen presenting function of dendritic cells via an action on host sialic acid-binding Ig-like lectin receptors. These receptors also induce suppression of CD4

T cells responses, and we presented evidence that the sialylation of parasite-derived mucins is required for the inhibitory effects on CD4 T cells. In this review we highlight the major mechanisms used by Trypanosoma cruzi to overcome host immunity and discuss the role of parasite colonization of the central thymic lymphoid tissue in chronic disease.

Autor: Ana Flávia Nardy, Célio Geraldo Freire-de-Lima, and Alexandre Morrot



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