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首页> 外文期刊>Microbes and infection >Atrophy of mesenteric lymph nodes in experimental Chagas' disease: differential role of Fas/Fas-L and TNFRI/TNF pathways.
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Atrophy of mesenteric lymph nodes in experimental Chagas' disease: differential role of Fas/Fas-L and TNFRI/TNF pathways.

机译：实验性恰加斯氏病中肠系膜淋巴结萎缩：Fas / Fas-L和TNFRI / TNF通路的不同作用。

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摘要

It is currently accepted that experimental acute infection by Trypanosoma cruzi promotes changes in secondary lymphoid organs, with general T and B lymphocyte polyclonal activation. Here we show that mesenteric lymph nodes (MLN) of acutely infected mice show severe atrophy due to extensive lymphocyte apoptosis. Accordingly, clusters of apoptotic cells are detected in the initial phase of infection in MLN but not in subcutaneous nodes. Moreover, such atrophy is independent of the infection route, parasite load or the mouse strain used. Studies in Fas-L deficient (BALB gld/gld+/+) and in TNF type 1 receptor (p55-/-) knockout mice indicate that both molecules are involved in MLN atrophy: Fas-L participates in cell death of CD4+ as well as B lymphocytes, whereas the TNF type 1 receptor is important for the apoptosis of CD4+ and CD8+ T lymphocytes. In contrast, perforin does not play a role, as lymph nodes from perforin-deficient mice do not behave differently from the corresponding wild types. Our data support the concept that, even in a systemic infection, differential (even opposing) responses can be found in different lymph node chains.
机译：目前公认的是，克氏锥虫的实验性急性感染可促进继发性淋巴器官的改变，并具有一般的T和B淋巴细胞多克隆激活作用。在这里，我们显示急性感染小鼠的肠系膜淋巴结（MLN）由于大量淋巴细胞凋亡而显示出严重的萎缩。因此，在MLN感染的初始阶段检测到凋亡细胞簇，但在皮下结节中未检测到。而且，这种萎缩与感染途径，寄生虫负荷或所用小鼠品系无关。 Fas-L缺乏（BALB gld / gld + / +）和TNF 1型受体（p55-/-）敲除小鼠的研究表明，这两种分子均与MLN萎缩有关：Fas-L参与CD4 +的细胞死亡以及B淋巴细胞，而TNF 1型受体对于CD4 +和CD8 + T淋巴细胞的凋亡很重要。相反，穿孔素不起作用，因为缺乏穿孔素的小鼠的淋巴结的行为与相应的野生型没有不同。我们的数据支持这样一个概念：即使在全身感染中，也可以在不同的淋巴结链中发现差异（甚至相反）的反应。

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