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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >Cutting edge: Identification of the thymic stromal lymphopoietin-responsive dendritic cell subset critical for initiation of type 2 contact hypersensitivity
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Cutting edge: Identification of the thymic stromal lymphopoietin-responsive dendritic cell subset critical for initiation of type 2 contact hypersensitivity

机译：前沿：确定对2型接触超敏反应至关重要的胸腺基质淋巴细胞生成素应答性树突状细胞亚群

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The cytokine thymic stromal lymphopoietin (TSLP) has been implicated in the initiation and progression of allergic inflammation through its ability to activate dendritic cells (DCs). However, the identity of the DC subset that responds to TSLP is not known. In this study we use a CCL17 reporter strain to identify the TSLPresponsiveDCsubset. In vitro, TSLP inducedCD11bhigh DCs to express CCL17, to increase CCR7-mediated migration activity, and to drive Th2 differentiation of naive CD4 T cells. In vivo, following skin sensitization, we found that a subset of Ag-bearing CCL17+CD11bhigh migratory DCs, but not Ag-bearing CCL172 migratory DCs, in skin lymph nodes were capable of driving Th2 differentiation and were dramatically reduced in TSLPR-deficient mice. Taken together, these results demonstrate that TSLP activated a subset of CD11b+ DCs in the skin to produce CCL17, upregulate CCR7, and migrate to the draining lymph node to initiate Th2 differentiation.
机译：细胞因子胸腺基质淋巴细胞生成素（TSLP）通过激活树突状细胞（DC）的能力而参与了过敏性炎症的发生和发展。但是，响应TSLP的DC子集的身份未知。在这项研究中，我们使用CCL17报告基因菌株鉴定TSLP responseDC亚集。在体外，TSLP诱导CD11b高DC表达CCL17，增加CCR7介导的迁移活性，并驱动天然CD4 T细胞的Th2分化。在体内，经皮肤敏化后，我们发现皮肤淋巴结中的一部分含Ag CCL17 + CD11b高迁移DC，而不是含Ag CCL172迁移DC能够驱动Th2分化，并在TSLPR缺陷小鼠中显着降低。综上所述，这些结果表明TSLP激活了皮肤中CD11b + DC的子集，从而产生CCL17，上调CCR7并迁移至引流淋巴结以启动Th2分化。

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