Dectin-1 mediates the biological effects of beta-glucans.

Dectin-1 mediates the biological effects of beta-glucans.
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Dectin-1介导β-葡聚糖的生物学作用。

DOI:
10.1084/jem.20021890
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发表时间:
2003-05-05
期刊:
The Journal of experimental medicine
影响因子:
--
通讯作者:
Gordon S
Gordon S
中科院分区:
其他
文献类型:
--
作者:
Brown GD;Herre J;Williams DL;Willment JA;Marshall AS;Gordon S

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真菌衍生的β-葡聚糖颗粒诱导白细胞活化和炎症介质(如肿瘤坏死因子(TNF)-α)产生的能力是一个很好的表征现象。尽管人们已经努力了解这些碳水化合物聚合物如何发挥其免疫调节作用,但参与产生这些反应的受体尚不清楚。在这里,我们发现Dectin-1介导对酶生酶和活真菌病原体的TNF-α的产生,这一活动发生在细胞表面,需要Dectin-1的细胞质尾部和免疫受体酪氨酸激活基元,以及toll样受体(TLR)-2和Myd88。这是首次证明,除了tlr外,对病原体的炎症反应还需要特定受体的识别。此外,这些研究表明Dectin-1在对真菌的反应中产生TNF-α,这是成功控制这些病原体所需的关键步骤。
The ability of fungal-derived β-glucan particles to induce leukocyte activation and the production of inflammatory mediators, such as tumor necrosis factor (TNF)-α, is a well characterized phenomenon. Although efforts have been made to understand how these carbohydrate polymers exert their immunomodulatory effects, the receptors involved in generating these responses are unknown. Here we show that Dectin-1 mediates the production of TNF-α in response to zymosan and live fungal pathogens, an activity that occurs at the cell surface and requires the cytoplasmic tail and immunoreceptor tyrosine activation motif of Dectin-1 as well as Toll-like receptor (TLR)-2 and Myd88. This is the first demonstration that the inflammatory response to pathogens requires recognition by a specific receptor in addition to the TLRs. Furthermore, these studies implicate Dectin-1 in the production of TNF-α in response to fungi, a critical step required for the successful control of these pathogens.
(1-> 3)-beta-d-d-Glucan免疫生物学的概述。
DOI: 10.1080/09629359791550
发表时间: 1997
影响因子: 4.6
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