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克氏锥虫逃避免疫反应,克氏锥虫是恰加斯病的病原体。

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

机构信息

Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.

出版信息

Braz J Med Biol Res. 2011 Feb;44(2):84-90. doi: 10.1590/s0100-879x2011007500005. Epub 2011 Jan 14.

DOI:10.1590/s0100-879x2011007500005
PMID:21243314
Abstract

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.

摘要

感染原生动物寄生虫克氏锥虫会导致查加斯病,该病影响拉丁美洲数百万人。免疫系统无法消除克氏锥虫感染。为了开发更有效的疫苗,需要更好地了解免疫逃避机制。在急性期,寄生虫大量复制并释放免疫调节分子,从而延迟 T 细胞介导的寄生虫特异性反应。这种免疫逃避使寄生虫在宿主中传播。在慢性期,寄生虫的逃避依赖于其劫持 TGF-β 信号通路的复制策略,该信号通路参与炎症和组织再生。本文综述了克氏锥虫的免疫逃避机制。

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