Basophils are known for their role in allergic inflammation, which makes them suitable targets in allergy diagnostics such as the basophil activation test (BAT) and the microfluidic immunoaffinity basophil activation test (miBAT). Beside their role in allergy, basophils have an immune modulatory role in both innate immunity and adaptive immunity. To accomplish this mission, basophils depend on the capability to migrate from blood to extravascular tissues, which includes interactions with endothelial cells, extracellular matrix and soluble mediators. Their receptor repertoire is well known, but less is known how these receptor–ligand interactions impact the degranulation process and the responsiveness to subsequent activation. As the consequences of these interactions are crucial to fully appreciate the role of basophils in immune modulation and to enable optimization of the miBAT, we explored how basophil activation status is regulated by cytokines and cross‐linking of adhesion molecules. The expression of adhesion molecules and activation markers on basophils from healthy blood donors was analysed by flow cytometry. Cross‐linking of CD203c, CD62L, CD11b and CD49d induced a significant upregulation of CD63 and CD203c. To mimic in vivo conditions, valid also for miBAT, CD62L and CD49d were cross‐linked followed by IgE‐dependent activation (anti‐IgE), which caused a reduced CD63 expression compared with anti‐IgE activation only. IL‐3 and IL‐33 priming caused increased CD63 expression after IgE‐independent activation (fMLP). Together, our data suggest that mechanisms operational both in the microfluidic chip and in vivo during basophil adhesion may impact basophil anaphylactic and piecemeal degranulation procedures and hence their immune regulatory function.

中文翻译：

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粘附分子交联和细胞因子暴露调节 IgE 和非 IgE 依赖性嗜碱性粒细胞活化。

嗜碱性粒细胞以其在过敏性炎症中的作用而闻名，这使它们成为过敏诊断中的合适靶点，例如嗜碱性粒细胞活化试验 (BAT) 和微流体免疫亲和嗜碱性粒细胞活化试验 (miBAT)。除了在过敏中的作用外，嗜碱性粒细胞在先天免疫和适应性免疫中都具有免疫调节作用。为了完成这一任务，嗜碱性粒细胞依赖于从血液迁移到血管外组织的能力，其中包括与内皮细胞、细胞外基质和可溶性介质的相互作用。它们的受体库是众所周知的，但鲜为人知的是这些受体-配体相互作用如何影响脱粒过程和对随后激活的反应。由于这些相互作用的结果对于充分理解嗜碱性粒细胞在免疫调节中的作用和优化 miBAT 至关重要，我们探索了细胞因子和粘附分子的交联如何调节嗜碱性粒细胞的激活状态。通过流式细胞术分析来自健康献血者的嗜碱性粒细胞上粘附分子和活化标志物的表达。CD203c、CD62L、CD11b 和 CD49d 的交联诱导 CD63 和 CD203c 的显着上调。为了模拟体内条件，对 miBAT 也有效，CD62L 和 CD49d 交联后进行 IgE 依赖性激活（抗 IgE），与仅抗 IgE 激活相比，这导致 CD63 表达降低。IL-3 和 IL-33 引发导致 IgE 非依赖性激活 (fMLP) 后 CD63 表达增加。一起，