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来自过敏供体的人血嗜碱性粒细胞中Toll样受体诱导的CXCL8分泌升高与Toll样受体表达水平无关。

Elevated Toll-Like Receptor-Induced CXCL8 Secretion in Human Blood Basophils from Allergic Donors Is Independent of Toll-Like Receptor Expression Levels.

作者信息

Steiner Markus, Hawranek Thomas, Schneider Michael, Ferreira Fatima, Horejs-Hoeck Jutta, Harrer Andrea, Himly Martin

机构信息

Department of Molecular Biology, University of Salzburg, Salzburg, Austria.

Laboratory for Immunological and Molecular Cancer Research, Paracelsus Medical University, Salzburg, Austria.

出版信息

PLoS One. 2016 Feb 12;11(2):e0149275. doi: 10.1371/journal.pone.0149275. eCollection 2016.

DOI:10.1371/journal.pone.0149275
PMID:26870962
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4752351/
Abstract

Human blood basophils have recently gained interest in addition to their function as allergic effector cells. Previous work suggests the involvement of innate immune mechanisms in the development and exacerbation of allergic responses, which might be mediated by basophils. We assayed the expression levels of Toll-like receptor (TLR) 1, 2, 4 and 6 on purified basophils from birch pollen-, house dust mite-, and non-allergic individuals. Additionally, we compared cytokine and chemokine secretion upon TLR stimulation in these basophil donor groups. Expression of TLR4 on the basophils of the allergic donor groups was decreased and CXCL8 secretion was elevated upon stimulation of TLR1/2 and TLR2/6 compared to the non-allergic donors. Decreased TLR expression and elevated CXCL8 secretion may represent possible mechanisms for aggravation of allergic symptoms in case of parasitic infection.

摘要

除了作为过敏效应细胞的功能外,人类血液嗜碱性粒细胞最近也受到了关注。先前的研究表明,先天免疫机制参与了过敏反应的发生和加剧,而这可能由嗜碱性粒细胞介导。我们检测了来自桦树花粉过敏、屋尘螨过敏和非过敏个体的纯化嗜碱性粒细胞上 Toll 样受体(TLR)1、2、4 和 6 的表达水平。此外,我们比较了这些嗜碱性粒细胞供体组在 TLR 刺激后细胞因子和趋化因子的分泌情况。与非过敏供体相比,过敏供体组嗜碱性粒细胞上 TLR4 的表达降低,并且在 TLR1/2 和 TLR2/6 刺激后 CXCL8 的分泌增加。TLR 表达降低和 CXCL8 分泌增加可能是寄生虫感染时过敏症状加重的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6115/4752351/8cb2777f2f68/pone.0149275.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6115/4752351/4c7bb9969cfa/pone.0149275.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6115/4752351/609f8d7b2b17/pone.0149275.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6115/4752351/274efdecbffe/pone.0149275.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6115/4752351/8cb2777f2f68/pone.0149275.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6115/4752351/4c7bb9969cfa/pone.0149275.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6115/4752351/609f8d7b2b17/pone.0149275.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6115/4752351/274efdecbffe/pone.0149275.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6115/4752351/8cb2777f2f68/pone.0149275.g004.jpg

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Activation of human basophils by combined toll-like receptor- and FcεRI-triggering can promote Th2 skewing of naive T helper cells.
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Front Pharmacol. 2016 Jun 17;7:171. doi: 10.3389/fphar.2016.00171. eCollection 2016.
联合 Toll 样受体和 FcεRI 触发可激活人嗜碱性粒细胞,从而促进幼稚 T 辅助细胞向 Th2 细胞的极化。
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