Objective

To synthesize investigations into the role of lipid-mediated recruitment and activation of group 2 innate lymphoid cells (ILC2s) in aspirin-exacerbated respiratory disease (AERD).

Data Sources

A comprehensive literature review of reports pertaining to cellular mechanisms, cytokine, and lipid mediators in AERD, as well as ILC2 activation and recruitment, was performed using PubMed and Google Scholar.

Study Selections

Selections of studies were based on reports of lipid mediators in AERD, cytokine mediators in AERD, type 2 effector cells in AERD, platelets in AERD, AERD treatment, ILC2s in allergic airway disease, and ILC2 activation, inhibition, and trafficking.

Results

The precise mechanisms of AERD pathogenesis are not well understood. Greater levels of proinflammatory lipid mediators and type 2 cytokines are found in tissues derived from patients with AERD relative to controls. After pathognomonic cyclooxygenase-1 inhibitor reactions, proinflammatory mediator concentrations (prostaglandin D2 and cysteinyl leukotrienes) are rapidly increased, as are ILC2 levels in the nasal mucosa. The ILC2s, which potently generate type 2 cytokines in response to lipid mediator stimulation, may play a key role in AERD pathogenesis.

Conclusion

Although the literature suggests that lipid-mediated ILC2 activation may occur in AERD, there is a dearth of definitive evidence. Future investigations leveraging novel next-generation single-cell sequencing approaches along with recently developed AERD murine models will better define lipid mediator–induced ILC2 trafficking in patients with AERD.

中文翻译：

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阿司匹林加剧的呼吸道疾病中脂质介导的先天淋巴细胞募集和激活

客观的

综合研究脂质介导的第 2 组先天淋巴细胞 (ILC2) 募集和激活在阿司匹林恶化的呼吸系统疾病 (AERD) 中的作用。

数据源

使用 PubMed 和 Google Scholar 对有关 AERD 中的细胞机制、细胞因子和脂质介质以及 ILC2 激活和募集的报告进行了全面的文献综述。

研究选择

研究的选择基于以下方面的报告：AERD 中的脂质介质、AERD 中的细胞因子介质、AERD 中的 2 型效应细胞、AERD 中的血小板、AERD 治疗、过敏性气道疾病中的 ILC2 以及 ILC2 激活、抑制和运输。

结果

AERD 发病机制的确切机制尚不清楚。与对照组相比，在 AERD 患者的组织中发现了更高水平的促炎脂质介质和 2 型细胞因子。发生特异性 cyclooxygenase-1 抑制剂反应后，促炎介质浓度（前列腺素 D2 和半胱氨酰白三烯）迅速升高，鼻粘膜中的 ILC2 水平也迅速升高。ILC2 可响应脂质介质刺激而有效产生 2 型细胞因子，可能在 AERD 发病机制中发挥关键作用。

结论

尽管文献表明脂质介导的 ILC2 激活可能发生在 AERD 中，但缺乏明确的证据。未来的研究利用新型下一代单细胞测序方法以及最近开发的 AERD 小鼠模型将更好地定义 AERD 患者中脂质介质诱导的 ILC2 贩运。