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首页> 外文期刊>Allergy >Natural killer-dendritic cell interaction in lymphocyte responses in hypersensitivity reactions to betalactams.
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Natural killer-dendritic cell interaction in lymphocyte responses in hypersensitivity reactions to betalactams.

机译：对β内酰胺的超敏反应中淋巴细胞反应中的自然杀伤树突状细胞相互作用。

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摘要

BACKGROUND: Betalactams are the commonest cause of allergic reactions mediated by either IgE or T lymphocytes in which innate and adaptive immune systems mediate the earlier stages of immunological responses. One of the links between these systems is related to the interaction between natural killer (NK) and dendritic cells (DC). We have evaluated the role of NK cells and NK-DC interaction in the immunopathological mechanisms of nonimmediate reactions to betalactams. METHODS: Patients allergic to amoxicillin (AX) (N = 17) and tolerant controls (N = 13) were included. Changes in phenotype (CD69, IFNgamma, perforin, and granzyme B) in AX-stimulated NK cells, the cytotoxic activity on mature or immature DC (imDC), and the proliferation and phenotype of NK lymphocytes after culture with AX and DC were determined by flow cytometry. RESULTS: Amoxicillin induced activation and increases of perforin and granzyme B (P = 0.007 and P = 0.041 respectively) but not IFNgamma production in NK cells from patients. In NK subpopulations, AX induced a significant enhancement of perforin and granzyme B in CD56(dim) (P = 0.005 and P = 0.002 respectively) and of IFNgamma in CD56(bright) (P = 0.001). The cytotoxic phenotype was demonstrated by an increase of annexin V only in imDC (P < 0.001). Amoxicillin also induced an increased NK proliferation with different patterns, cytotoxic or proinflammatory, depending on the presence of imDC or mature DC, respectively. No differences were observed in NK cells from tolerant controls. CONCLUSION: These data could demonstrate the involvement of NK cells in the immunopathological mechanisms of nonimmediate allergic reactions to AX, showing that both the innate and adaptive immune systems are involved and crosstalk, producing amplification of the harmful effects observed in these drug reactions.
机译：背景：内酰胺类是由IgE或T淋巴细胞介导的过敏反应的最常见原因，其中先天和适应性免疫系统介导免疫反应的早期阶段。这些系统之间的联系之一与自然杀手（NK）和树突状细胞（DC）之间的相互作用有关。我们已经评估了NK细胞和NK-DC相互作用在非直接反应β-内酰胺类的免疫病理机制中的作用。方法：包括对阿莫西林（AX）过敏的患者（N = 17）和耐受性对照（N = 13）。 AX刺激的NK细胞的表型（CD69，IFNgamma，穿孔素和颗粒酶B）的变化，在成熟或未成熟的DC（imDC）上的细胞毒活性以及AX和DC培养后NK淋巴细胞的增殖和表型通过流式细胞仪。结果：阿莫西林诱导了患者NK细胞中穿孔素和颗粒酶B的激活和增高（分别为P = 0.007和P = 0.041），但没有IFNγ的产生。在NK亚群中，AX诱导CD56（dim）中的穿孔素和颗粒酶B显着增强（分别为P = 0.005和P = 0.002）和CD56（亮）中的IFNgamma（P = 0.001）。仅在imDC中膜联蛋白V的增加证明了细胞毒性表型（P <0.001）。阿莫西林还分别根据imDC或成熟DC的存在，以不同的模式（细胞毒性或促炎性）诱导NK增殖增加。与耐受性对照相比，NK细胞未见差异。结论：这些数据可以证明NK细胞参与了对AX的非立即性过敏反应的免疫病理机制，表明先天和适应性免疫系统均参与并串扰，从而放大了在这些药物反应中观察到的有害作用。

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