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肺脏 CD103(+)树突状细胞对吸入性变应原引发 Th2 反应。

Pulmonary CD103(+) dendritic cells prime Th2 responses to inhaled allergens.

机构信息

Laboratory of Respiratory Biology, Division of Intramural Research, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina, USA.

出版信息

Mucosal Immunol. 2012 Jan;5(1):53-65. doi: 10.1038/mi.2011.47. Epub 2011 Oct 19.

Abstract

Allergic asthma stems largely from the actions of T helper 2 (Th2) cells, but the pathways that initiate Th2 responses to inhaled allergens are not fully understood. In the lung, there are two major subsets of dendritic cells (DCs), displaying CD11b or CD103. We found that after taking up inhaled ovalbumin in vivo, purified CD103(+) DCs from the lung or lung-draining lymph nodes primed Th2 differentiation ex vivo. Th2 induction by CD103(+) DCs was also seen when cockroach or house dust mite allergens were used. In contrast, CD11b(hi) DCs primed Th1 differentiation. Moreover, mice lacking CD103(+) DCs displayed diminished Th2 priming to various inhaled allergens and did not develop asthma-like responses following subsequent allergen challenge. Low-level antigen presentation by CD103(+) DCs was necessary, but not sufficient for Th2 priming. Together, these findings show that CD103(+) DCs have a significant role in priming Th2 responses to inhaled allergens.

摘要

过敏性哮喘主要源于辅助性 T 细胞 2(Th2)细胞的作用,但引发 Th2 对吸入性过敏原产生反应的途径尚未完全阐明。在肺部,有两种主要的树突状细胞(DC)亚群,分别表达 CD11b 或 CD103。我们发现,在体内摄取吸入性卵清蛋白后,来自肺部或引流淋巴结的纯化 CD103(+) DC 可在体外引发 Th2 分化。当使用蟑螂或屋尘螨过敏原时,也观察到 CD103(+) DC 诱导 Th2 分化。相比之下,CD11b(hi) DC 可引发 Th1 分化。此外,缺乏 CD103(+) DC 的小鼠对各种吸入性过敏原的 Th2 引发作用减弱,并且在随后的过敏原挑战后不会发展为哮喘样反应。CD103(+) DC 的低水平抗原呈递对于 Th2 引发是必要的,但不是充分的。总之,这些发现表明 CD103(+) DC 在引发对吸入性过敏原的 Th2 反应中具有重要作用。

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