Distant lymph nodes serve as pools of Th1 cells induced by neonatal BCG vaccination for the prevention of asthma in mice

Distant lymph nodes serve as pools of Th1 cells induced by neonatal BCG vaccination for the prevention of asthma in mice
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DOI:
10.1111/all.12099
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发表时间:
2013-03-01
期刊:
影响因子:
12.4
通讯作者:
Shen, H.
Shen, H.
中科院分区:
医学1区
文献类型:
--
作者:
Zhang, G.;Wang, P.;Shen, H.

文献摘要

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背景新生儿卡介苗(BCG)疫苗接种可诱导强烈的Th 1型辅助性T细胞应答并抑制过敏相关的气道功能障碍,但其确切机制尚不清楚。本研究的目的是探讨新生儿卡介苗接种诱导的Th 1细胞在哪里产生和储存,以及它们如何被招募到发炎的气道中以预防过敏原诱导的气道炎症。方法采用新生C57 BL/6小鼠接种卡介苗,建立哮喘小鼠模型,观察其体内、外Th 1细胞的表达和功能。结果BCG疫苗可诱导小鼠腹股沟淋巴结(ILN)局部Th 1细胞向肺内迁移。ILN中的这些CD 4 + T细胞表现出活化、增殖和细胞因子分泌的潜力,并表达高水平的CXCR 3。从BCG处理的ILN中连续转移的CD 4 + T细胞显著降低过敏性气道反应。此外,卡介苗接种对过敏性气道炎症的保护作用在ILN切除后丧失。结论ILN在BCG免疫后可作为Th 1细胞的“武器库”,在过敏原刺激下,ILN可迁移至炎症肺,从而抑制过敏原诱导的气道疾病。
Background Neonatal Bacillus CalmetteGuerin (BCG) vaccination induces vigorous T-helper type 1 (Th1) responses and inhibits allergy-related airway dysfunction, but the exact mechanisms remain unclear. The objective of this study was to address where the Th1 cells induced by neonatal BCG vaccination are generated and stored, and how they are recruited into the inflamed airway for the prevention of allergen-induced airway inflammation. Methods We vaccinated neonatal C57BL/6 mice with BCG in a mouse model of asthma and analyzed the expression and function of Th1 cells in vivo and in vitro. Results BCG vaccinationinduced Th1 cells in the local inguinal lymph nodes (ILN) migrated into the lungs upon inhaled ovalbumin (OVA) challenge in OVA-sensitized mice. These CD4+ T cells in the ILN exhibited potentials of activation, proliferation and cytokine secretion and expressed high levels of CXCR3. Adoptive transfer of CD4+ T cells from BCG-treated ILN significantly decreased allergic airway responses. In addition, the protective effect of BCG vaccination against allergic airway inflammation was lost upon the excision of the ILN. Conclusions These data demonstrate that ILN serves as a weapon' pool of Th1 cells following BCG vaccination, and these cells are ready for the migration into the inflamed lungs upon the allergen challenge, thereby inhibiting allergen-induced airway disorder.