Evasion of immune responses by Trypanosoma cruzi, the etiological agent of Chagas disease

被引:9
作者
DosReis, G. A. [1 ,2 ]
机构
[1] UFRJ, CCS, Inst Biofis Carlos Chagas Filho, BR-21949900 Rio De Janeiro, Brazil
[2] Conselho Nacl Desenvolvimento Cient & Tecnol, Inst Nacl Saude & Ambiente Regiao Amazon, Brasilia, DF, Brazil
关键词
Trypanosoma cruzi; T cells; GPI-anchors; TGF-beta; Mucin; Apoptosis; T-CELL RESPONSES; TOLL-LIKE RECEPTOR-2; GROWTH-FACTOR-BETA; TGF-BETA; IN-VITRO; DENDRITIC CELLS; TRANS-SIALIDASE; CUTTING EDGE; INFECTION; APOPTOSIS;
D O I
10.1590/S0100-879X2011007500005
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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-beta signaling pathway involved in inflammation and tissue regeneration. In this article, the mechanisms of immune evasion described for T. cruzi are reviewed.
引用
收藏
页码:84 / 90
页数:7
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