Dysregulation of macrophage signal transduction by Toxoplasma gondii: past progress and recent advances.

Dysregulation of macrophage signal transduction by Toxoplasma gondii: past progress and recent advances.
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DOI:
10.1111/j.1365-3024.2009.01122.x
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发表时间:
2009-12
影响因子:
2.2
通讯作者:
Denkers EY
Denkers EY
中科院分区:
医学4区
文献类型:
--
作者:
Leng J;Butcher BA;Denkers EY

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机会性原生动物寄生虫刚地弓形虫是众所周知的细胞介导免疫的强诱导剂,主要是由于体内感染过程中促炎细胞因子的诱导。然而,在细胞内感染期间,寄生虫抑制导致这些促炎反应的信号转导途径。相反的反应可能反映了寄生虫需要刺激免疫以允许宿主生存和寄生虫持续存在,同时避免过度的反应,可能导致寄生虫消除和宿主免疫病理。本文综述了弓形虫对宿主细胞信号转导的影响。这些研究揭示了寄生虫感染巨噬细胞和其他先天免疫细胞时发生的促炎细胞因子反应的深刻抑制。
The opportunistic protozoan parasite Toxoplasma gondii is well known as a strong inducer of cell-mediated immunity, largely as a result of proinflammatory cytokine induction during in vivo infection. Yet, during intracellular infection the parasite suppresses signal transduction pathways leading to these proinflammatory responses. The opposing responses are likely to reflect the parasite's need to stimulate immunity allowing host survival and parasite persistence, and at the same time avoiding excessive responses that could result in parasite elimination and host immunopathology. This Review summarizes past and present investigations into the effects of Toxoplasma on host cell signal transduction. These studies reveal insight into the profound suppression of proinflammatory cytokine responses that occurs when the parasite infects macrophages and other cells of innate immunity.
感染期间淋巴结中中性粒细胞迁移的动态。
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