CD4(+) T-cell survival in the GI tract requires dectin-1 during fungal infection.
CD4(+) T-cell survival in the GI tract requires dectin-1 during fungal infection.
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DOI：
10.1038/mi.2015.79
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发表时间：
2016-03
影响因子：
8
通讯作者：
Brown GD
中科院分区：
文献类型：
--
作者：
Drummond RA;Dambuza IM;Vautier S;Taylor JA;Reid DM;Bain CC;Underhill DM;Masopust D;Kaplan DH;Brown GD
Dectin-1 是一种天然抗真菌 C 型凝集素受体，是保护性抗真菌免疫所必需的。我们最近发现 Dectin-1 参与控制胃肠道 (GI) 的真菌感染，但这种 C 型凝集素受体如何介导这些活动尚不清楚。在这里，我们证明 Dectin-1 对于驱动胃肠道中真菌特异性 CD4+ T 细胞反应至关重要。 Dectin-1 的缺失导致肠系膜淋巴结 (mLN) 中的树突状细胞反应消失和 T 细胞共刺激缺陷，导致 CD4+ T 细胞凋亡大幅增加和胃肠道相关淋巴组织的细胞结构减少。 CD8+ T 细胞反应不受 Dectin-1 缺陷的影响。 Dectin-1 的这些功能对于我们了解肠道免疫和真菌感染的易感性具有重要意义。
Dectin-1 is an innate antifungal C-type lectin receptor necessary for protective antifungal immunity. We recently discovered that Dectin-1 is involved in controlling fungal infections of the gastrointestinal (GI) tract, but how this C-type lectin receptor mediates these activities is unknown. Here, we show that Dectin-1 is essential for driving fungal-specific CD4+ T-cell responses in the GI tract. Loss of Dectin-1 resulted in abrogated dendritic cell responses in the mesenteric lymph nodes (mLNs) and defective T-cell co-stimulation, causing substantial increases in CD4+ T-cell apoptosis and reductions in the cellularity of GI-associated lymphoid tissues. CD8+ T-cell responses were unaffected by Dectin-1 deficiency. These functions of Dectin-1 have significant implications for our understanding of intestinal immunity and susceptibility to fungal infections.