Trogocytosis with monocytes associated with increased α2,3 sialic acid expression on B cells during H5N1 influenza virus infection.

Trogocytosis with monocytes associated with increased α2,3 sialic acid expression on B cells during H5N1 influenza virus infection.
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DOI:
10.1371/journal.pone.0239488
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发表时间:
2020
期刊:
影响因子:
3.7
通讯作者:
Thitithanyanont A
Thitithanyanont A
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Kongsomros S;Thanunchai M;Manopwisedjaroen S;Na-Ek P;Wang SF;Taechalertpaisarn T;Thitithanyanont A

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H5N1病毒引起跨物种感染并导致人类高死亡率,其免疫发病机制已得到深入研究。我们之前观察到单核细胞和B细胞之间的相互作用,共培养后增加了B细胞对H5N1病毒感染的易感性。在该共培养模型中,B 细胞表面的 α2,3 唾液酸(禽流感受体)水平也显着增加,但解释尚不清楚。在这项研究中,我们旨在确定 B 细胞上 α2,3 唾液酸增加的可能机制。提出了 B 细胞通过细胞接触依赖性吞噬作用获得 α2,3 SA。结果显示,B细胞表面缺乏α2,3 SA,并且B细胞从H5N1感染的共培养物中的单核细胞获得膜结合的α2,3 SA分子。膜交换的发生主要依赖于 H5N1 感染和细胞间接触,而不是模拟感染和 Transwell。 B 细胞表面 α2,3 SA 的增加由 trogocytosis 介导,与 H5N1 感染的易感性增强有关。因此,这些观察结果证明,尽管缺乏禽流感受体,H5N1流感病毒可能利用胞吞作用来扩大其细胞向性并传播至免疫细胞。
The immunopathogenesis of H5N1 virus has been studied intensively since it caused cross-species infection and induced high mortality to human. We previously observed the interaction between monocytes and B cells, which increased the susceptibility of B cell to H5N1 virus infection after a co-culture. Levels of α2,3 sialic acid (avian flu receptor) were also significantly increased on B cell surface in this co-culture model with unclear explanation. In this study, we aimed to determine the possible mechanism that responded for this increase in α2,3 sialic acid on B cells. Acquisition of α2,3 SA by B cells via cell contact-dependent trogocytosis was proposed. Results showed that the lack of α2,3 SA was detected on B cell surface, and B cells acquired membrane-bound α2,3 SA molecules from monocytes in H5N1-infected co-cultures. Occurrence of membrane exchange mainly relied on H5N1 infection and cell-cell contact as opposed to a mock infection and transwell. The increase in α2,3 SA on B cell surface mediated by trogocytosis was associated with the enhanced susceptibility to H5N1 infection. These observations thus provide the evidence that H5N1 influenza virus may utilize trogocytosis to expand its cell tropism and spread to immune cells despite the lack of avian flu receptor.
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