美国西奈山伊坎医学院Shruti Naik团队的一项最新研究发现了外周免疫诱导树突状细胞驱动早期过敏性炎症。相关论文于2026年2月25日发表于国际顶尖学术期刊《自然》杂志上。

在这里，该团队发现，在生命早期，暴露于常见的过敏原会引发明显的分叉免疫反应，同时引发皮肤中的17型炎症，并在淋巴结中启动典型的T辅助2致敏。这种早期γδ 17型介导的皮炎在继发性变应原暴露后引发了严重的变应性肺部炎症。在机制上，课题组人员发现树突状细胞（DC）介导的17型激活直接在皮肤中进行，而不需要迁移到淋巴结；课题组人员将这种状态称为“外周免疫诱导”（pii） DC。CD301b⁺常规2型DCs获得过敏原，采用pii-DC状态，产生IL-23，并独立于淋巴结接合激活局部γδ 17型细胞。pii-DC状态是由未成熟的下丘脑-垂体-肾上腺轴和早期生理低系统性糖皮质激素特征所激活的；DC特异性糖皮质激素受体的缺失再现了pii-DC表型。这些发现定义了一个发育检查点，由神经内分泌成熟设定，使原位DC激活和免疫诱导成为可能，从而形成对过敏原的年龄依赖性反应。

据了解，与过敏原相关的特应性疾病以及过敏性疾病经常在生命早期出现；然而，控制对过敏原免疫反应的年龄依赖性机制仍然知之甚少。

附：英文原文

Title: Peripheral immune-inducer dendritic cells drive early-life allergic inflammation

Author: Xing, Yue, Reznikov, Ilana, Ahmed, Abonti Nur, Sidhu, Ikjot, Wisnewski, Jill, Farhat, Asma, Prystupa, Aleksandr, Konieczny, Piotr, Mansfield, Kody, Cooper, Melissa L., Yeung, Stephen T., Kim, Madeline, Adeghe, Sophia, Gaines, Katherine D., Manson, Meredith, Sim, Ji Hyun, Huang, Qingrong, Moshiri, Ata S., Khanna, Kamal M., Lu, Theresa T., Guttman-Yassky, Emma, Lund, Amanda W., Anandasabapathy, Niroshana, Naik, Shruti

Issue&Volume: 2026-02-25

Abstract: Atopic diseases associated with allergens, as well as allergic diseases, frequently arise early in life; however, the age-dependent mechanisms governing immune responses to allergens remain poorly understood1. Here we find that in early life, exposure to common allergens triggers a distinct bifurcated immune response, simultaneously triggering type 17 inflammation in the skin and initiating canonical T helper 2 sensitization in the lymph nodes. This early-life γδ type 17-mediated dermatitis primes the exaggerated allergic lung inflammation upon secondary allergen exposure. Mechanistically, we find dendritic cell (DC)-mediated type 17 activation directly in the skin without requiring migration to lymph nodes; we term this state ‘peripheral immune inducer’ (pii) DC. CD301b+ conventional type 2 DCs acquire allergen, adopt the pii-DC state, produce IL-23 and activate local γδ type 17 cells independently of lymph-node engagement. The pii-DC state is enabled by the immature hypothalamic–pituitary–adrenal axis and physiologically low systemic glucocorticoids characteristic of early life2,3; DC-specific deletion of the glucocorticoid receptor recapitulates the pii-DC phenotype. These findings define a developmental checkpoint, set by neuroendocrine maturation, that enables in situ DC activation and immune induction, thereby shaping age-dependent responses to allergens.

DOI: 10.1038/s41586-026-10162-x

Source: https://www.nature.com/articles/s41586-026-10162-x