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本文引用的文献

1
Roles of OX40 in the development of murine experimental allergic conjunctivitis: exacerbation and attenuation by stimulation and blocking of OX40.OX40在小鼠实验性变应性结膜炎发展中的作用:OX40刺激和阻断导致病情加重与减轻
Invest Ophthalmol Vis Sci. 2006 Feb;47(2):657-63. doi: 10.1167/iovs.05-1064.
2
The interaction between ICOS and B7RP-1 is not required for the development of experimental murine allergic conjunctivitis.ICOS与B7RP-1之间的相互作用对于实验性小鼠变应性结膜炎的发展并非必需。
Biochem Biophys Res Commun. 2005 Dec 30;338(4):1726-31. doi: 10.1016/j.bbrc.2005.10.177. Epub 2005 Nov 7.
3
The control of allergic conjunctivitis by suppressor of cytokine signaling (SOCS)3 and SOCS5 in a murine model.细胞因子信号转导抑制因子(SOCS)3和SOCS5在小鼠模型中对变应性结膜炎的调控作用
J Immunol. 2005 Oct 15;175(8):5489-97. doi: 10.4049/jimmunol.175.8.5489.
4
Engagement of 4-1BB inhibits the development of experimental allergic conjunctivitis in mice.4-1BB的激活抑制小鼠实验性变应性结膜炎的发展。
J Immunol. 2005 Oct 15;175(8):4897-903. doi: 10.4049/jimmunol.175.8.4897.
5
Genetic background determines susceptibility to experimental immune-mediated blepharoconjunctivitis: comparison of Balb/c and C57BL/6 mice.遗传背景决定实验性免疫介导性睑结膜炎的易感性:Balb/c小鼠和C57BL/6小鼠的比较。
Exp Eye Res. 2006 Feb;82(2):210-8. doi: 10.1016/j.exer.2005.06.010. Epub 2005 Aug 18.
6
The B7 family revisited.重新审视B7家族。
Annu Rev Immunol. 2005;23:515-48. doi: 10.1146/annurev.immunol.23.021704.115611.
7
Predominance of infiltrating IL-4-producing T cells in conjunctiva of patients with allergic conjunctival disease.过敏性结膜疾病患者结膜中产生白细胞介素-4的浸润性T细胞占优势。
Curr Eye Res. 2004 Oct-Nov;29(4-5):235-43. doi: 10.1080/02713680490516738.
8
Paradoxical role of programmed death-1 ligand 2 in Th2 immune responses in vitro and in a mouse asthma model in vivo.程序性死亡-1配体2在体外Th2免疫反应及体内小鼠哮喘模型中的矛盾作用。
Eur J Immunol. 2004 Dec;34(12):3326-36. doi: 10.1002/eji.200425197.
9
B7-DC regulates asthmatic response by an IFN-gamma-dependent mechanism.B7-DC 通过一种依赖干扰素-γ 的机制调节哮喘反应。
J Immunol. 2004 Feb 15;172(4):2530-41. doi: 10.4049/jimmunol.172.4.2530.
10
Preferential contribution of B7-H1 to programmed death-1-mediated regulation of hapten-specific allergic inflammatory responses.B7-H1对程序性死亡-1介导的半抗原特异性过敏性炎症反应调节的优先贡献。
Eur J Immunol. 2003 Oct;33(10):2773-82. doi: 10.1002/eji.200324084.

程序性死亡配体2(PD-L2)在小鼠实验性变应性结膜炎发病中的作用

Involvement of programmed death-ligand 2 (PD-L2) in the development of experimental allergic conjunctivitis in mice.

作者信息

Fukushima A, Yamaguchi T, Azuma M, Yagita H, Ueno H

机构信息

Department of Ophthalmology, Kochi Medical School, Kochi University, Kohasu, Oko-cho, Nankoku-city 783-8505, Japan.

出版信息

Br J Ophthalmol. 2006 Aug;90(8):1040-5. doi: 10.1136/bjo.2006.091314. Epub 2006 Apr 13.

DOI:10.1136/bjo.2006.091314
PMID:16613922
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1857191/
Abstract

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.

摘要

背景/目的:程序性死亡-1(PD-1)及其配体在实验性变应性气道疾病中的作用已得到证实。在此,作者旨在研究PD-1及其配体是否参与小鼠实验性变应性结膜炎(EC)的发生发展。

方法

通过在明矾中用短豚草花粉(RW)主动免疫Balb/c小鼠诱导EC。10天后(第10天),用含RW的滴眼液对小鼠进行激发。激发后24小时,采集结膜、脾脏和血清进行组织学分析、细胞因子检测以及RW特异性Ig水平测定。在诱导期(第0、2、4、6和8天)或效应期(第10天RW激发前2小时),对主动免疫的小鼠用抗PD-1、抗PD-L1、抗PD-L2抗体(Abs)或正常大鼠免疫球蛋白G(nrIgG)进行治疗。

结果

诱导期抗体治疗虽可调节免疫反应,但不影响嗜酸性粒细胞浸润。相反,效应期用抗PD-L2抗体而非抗PD-1或抗PD-L1抗体治疗可显著增加结膜中嗜酸性粒细胞浸润,且不影响全身免疫反应。

结论

与变应性气道炎症相似,PD-L2在效应期而非诱导期参与EC的发生发展。