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首页> 外文期刊>British journal of ophthalmology >Involvement of programmed death-ligand 2 (PD-L2) in the development of experimental allergic conjunctivitis in mice.
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Involvement of programmed death-ligand 2 (PD-L2) in the development of experimental allergic conjunctivitis in mice.

机译:程序性死亡配体2(PD-L2)参与小鼠实验性过敏性结膜炎的发展。

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BACKGROUND/AIM: Involvement of programmed death-1 (PD-1) and its ligands has been demonstrated in experimental allergic airway disease. Here, the authors aimed to examine whether PD-1 and its ligands are involved in the development of experimental allergic conjunctivitis (EC) in mice. METHODS: EC was induced in Balb/c mice by active immunisation with short ragweed pollen (RW) in alum. 10 days later (day 10), the mice were challenged with eye drops containing RW. 24 hours after the challenge, conjunctivas, spleens, and sera were harvested for histological analysis, cytokine assays, and measurement of RW specific Ig levels. The actively immunised mice were treated with anti-PD-1, anti-PD-L1, anti-PD-L2 antibodies (Abs), or normal rat immunoglobulin G (nrIgG) during either the induction (day 0, 2, 4, 6, and 8) or the effector (2 hours before RW challenge on day 10) phase. RESULTS: Ab treatment during the induction phase did not affect eosinophil infiltration although immune responses were modulated. In contrast, treatment with anti-PD-L2 Ab, but not anti-PD-1 or anti-PD-L1 Ab, during the effector phase significantly increased eosinophil infiltration into the conjunctiva without affecting systemic immune responses. CONCLUSIONS: Similar to allergic airway inflammation, PD-L2 is involved in the development of EC during the effector phase but not the induction phase.
机译:背景/目的:在实验性过敏性气道疾病中已证明参与程序性死亡1(PD-1)及其配体的参与。在这里,作者旨在检查PD-1及其配体是否参与小鼠实验性过敏性结膜炎(EC)的发展。方法:在明矾中通过短豚草花粉(RW)主动免疫在Balb / c小鼠中诱导EC。 10天后(第10天),用含RW的滴眼液攻击小鼠。攻击后24小时,收获结膜,脾和血清用于组织学分析,细胞因子测定和RW特异性Ig水平的测量。主动免疫的小鼠在诱导过程中(第0、2、4、6天)均用抗PD-1,抗PD-L1,抗PD-L2抗体(Abs)或正常大鼠免疫球蛋白G(nrIgG)治疗,以及8)或效应器(第10天进行RW挑战前2小时)阶段。结果:尽管免疫反应受到调节,诱导期的抗体治疗并没有影响嗜酸性粒细胞的浸润。相反,在效应期用抗PD-L2 Ab进行治疗,而不用抗PD-1或抗PD-L1 Ab进行治疗,可显着增加嗜酸性粒细胞向结膜的浸润,而不会影响全身免疫反应。结论:与过敏性气道炎症相似,PD-L2在效应期而不是诱导期参与EC的发展。

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