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Novel cooperation between CX3CL1 and CCL26 inducing NK cell chemotaxis via CX3CR1: A possible mechanism for NK cell infiltration of the allergic nasal tissue

机译：CX3CL1和CCL26之间通过CX3CR1诱导NK细胞趋化性的新合作：NK细胞浸润过敏性鼻组织的可能机制

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Background: Recent data indicated that natural killer (NK) cells and chemokines could play a pivotal role in nasal inflammation. CX3CR1, the only receptor for fractalkine/CX3CL1, is abundantly expressed by NK cells, and was recently shown to also be a receptor for eotaxin-3/CCL26. However, no reports explored the NK cells-CX3CL1-CCL26 axis via CX3CR1 in allergy. Objective: Our goals were first to determine specifically NK cell recruitment pattern in nasal tissue of allergic chronic rhinosinusitis (ACRS) and non-allergic chronic rhinosinusitis (NACRS) patients in comparison with healthy controls, and secondly, to investigate the function of CX3CR1 in NK cell migration. Methods: Immunohistochemistry, microchemotaxis chambers, flow cytometry and confocal microscopy were used in this study. Results: Herein, we showed that NK cells infiltrated the epithelial layers of nasal tissue only in ACRS patients and not in NACRS patients or controls. NK cells were also more numerous in the stroma of the nasal tissue from ACRS patients compared with NACRS patients or controls. This migration could be mediated by both CX3CL1 and CCL26, as these two chemokines induced NK cell migration. Moreover, both molecules also stimulated cytoskeleton changes and F-actin reorganisation in NK cells. Chemotaxis and cytoskeleton changes were sensitive to genistein, a tyrosine kinase inhibitor. By flow cytometry, we demonstrated that a single antigen nasal provocation challenge increased the expression of CX3CR1 on NK cells in allergic rhinitis (AR) patients. The function of this receptor was associated with a significant augmentation of NK cell chemotaxis against the optimal doses of CX3CL1 and CCL26. Conclusions and Clinical Relevance: Our results highlight a novel role for CX3CR1 in NK cell migration that may contribute to the NK cell trafficking to the allergic upper airway. This could be mediated largely by CX3CL1 and CCL26 stimulation of the tyrosine kinase pathway. ? 2012 Blackwell Publishing Ltd.
机译：背景：最新数据表明，自然杀伤（NK）细胞和趋化因子可能在鼻炎症中起关键作用。 CX3CR1是fractalkine / CX3CL1的唯一受体，在NK细胞中大量表达，并且最近也被证明是eotaxin-3 / CCL26的受体。然而，没有报道通过变态反应通过CX3CR1探索NK细胞-CX3CL1-CCL26轴。目的：我们的目标是首先确定过敏性慢性鼻-鼻窦炎（ACRS）和非过敏性慢性鼻-鼻窦炎（NACRS）患者鼻腔组织中NK细胞募集模式，与健康对照组进行比较;其次，研究CX3CR1在NK中的功能细胞迁移。方法：采用免疫组织化学，微趋化室，流式细胞术和共聚焦显微镜。结果：在本文中，我们显示NK细胞仅在ACRS患者而非NACRS患者或对照中浸润鼻组织的上皮层。与NACRS患者或对照组相比，ACRS患者鼻腔组织中的NK细胞数量也更多。该迁移可能由CX3CL1和CCL26介导，因为这两个趋化因子诱导NK细胞迁移。而且，这两种分子还刺激NK细胞中的细胞骨架变化和F-肌动蛋白重组。趋化性和细胞骨架变化对染料木黄酮（酪氨酸激酶抑制剂）敏感。通过流式细胞仪，我们证明了在过敏性鼻炎（AR）患者中，单抗原鼻激发挑战增加了NK细胞上CX3CR1的表达。该受体的功能与针对最佳剂量的CX3CL1和CCL26的NK细胞趋化性显着增加有关。结论和临床意义：我们的结果突出了CX3CR1在NK细胞迁移中的新作用，这可能有助于NK细胞向过敏性上呼吸道的运输。这可能主要由酪氨酸激酶途径的CX3CL1和CCL26刺激介导。 ？ 2012布莱克威尔出版有限公司

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