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Complement anaphylatoxin receptors C3aR and C5aR are required in the pathogenesis of experimental autoimmune uveitis.补体过敏毒素受体C3aR和C5aR在实验性自身免疫性葡萄膜炎的发病机制中是必需的。
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Complement anaphylatoxin receptors C3aR and C5aR are required in the pathogenesis of experimental autoimmune uveitis.补体过敏毒素受体C3aR和C5aR在实验性自身免疫性葡萄膜炎的发病机制中是必需的。
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本文引用的文献

1
New developments in C5a receptor signaling.C5a受体信号传导的新进展。
Cell Health Cytoskelet. 2012 Jul 1;4:73-82. doi: 10.2147/CHC.S27233. Epub 2012 Jul 31.
2
C5L2: a controversial receptor of complement anaphylatoxin, C5a.C5L2：补体过敏毒素 C5a 的有争议受体。
FASEB J. 2013 Mar;27(3):855-64. doi: 10.1096/fj.12-220509. Epub 2012 Dec 13.
3
Cytokines in autoimmune uveitis.自身免疫性葡萄膜炎中的细胞因子。
J Interferon Cytokine Res. 2011 Oct;31(10):733-44. doi: 10.1089/jir.2011.0042. Epub 2011 Jul 25.
4
Inhibiting the C5-C5a receptor axis.抑制 C5-C5a 受体轴。
Mol Immunol. 2011 Aug;48(14):1631-42. doi: 10.1016/j.molimm.2011.04.014. Epub 2011 May 6.
5
Systemic and local anti-C5 therapy reduces the disease severity in experimental autoimmune uveoretinitis.系统性和局部抗 C5 治疗可降低实验性自身免疫性葡萄膜炎的疾病严重程度。
Clin Exp Immunol. 2010 Mar;159(3):303-14. doi: 10.1111/j.1365-2249.2009.04070.x. Epub 2009 Dec 4.
6
The dynamics of leukocyte infiltration in experimental autoimmune uveoretinitis.实验性自身免疫性葡萄膜视网膜炎中白细胞浸润的动态变化
Prog Retin Eye Res. 2008 Sep;27(5):527-35. doi: 10.1016/j.preteyeres.2008.07.001. Epub 2008 Aug 3.
7
Complement-targeted therapeutics.补体靶向疗法。
Nat Biotechnol. 2007 Nov;25(11):1265-75. doi: 10.1038/nbt1342.
8
The role of complement system in ocular diseases including uveitis and macular degeneration.补体系统在包括葡萄膜炎和黄斑变性在内的眼部疾病中的作用。
Mol Immunol. 2007 Sep;44(16):3901-8. doi: 10.1016/j.molimm.2007.06.145.
9
Genetic deficiency of C3 as well as CNS-targeted expression of the complement inhibitor sCrry ameliorates experimental autoimmune uveoretinitis.C3的基因缺陷以及补体抑制剂sCrry在中枢神经系统的靶向表达可改善实验性自身免疫性葡萄膜视网膜炎。
Exp Eye Res. 2006 Mar;82(3):389-94. doi: 10.1016/j.exer.2005.07.011. Epub 2005 Sep 6.
10
Uveitis: a potentially blinding disease.葡萄膜炎：一种可能致盲的疾病。
Ophthalmologica. 2004 Jul-Aug;218(4):223-36. doi: 10.1159/000078612.

补体过敏毒素受体对于实验性自身免疫性葡萄膜炎的发展并非必需。

The complement anaphylatoxin receptors are not required for the development of experimental autoimmune uveitis.

机构信息

Department of Ophthalmology, The University of Alabama at Birmingham, 1530 3rd Avenue South, Birmingham, AL 35294-1150, USA; Department of Pathology, The University of Alabama at Birmingham, 1530 3rd Avenue South, Birmingham, AL 35294-1150, USA; Department of Microbiology, The University of Alabama at Birmingham, 1530 3rd Avenue South, Birmingham, AL 35294-1150, USA.

出版信息

J Neuroimmunol. 2013 Nov 15;264(1-2):127-9. doi: 10.1016/j.jneuroim.2013.08.010. Epub 2013 Aug 31.

DOI:10.1016/j.jneuroim.2013.08.010
PMID:24035596
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3818408/
Abstract

To determine if complement anaphylatoxin-mediated inflammation contributes to the development and progression of experimental autoimmune uveitis (EAU), we induced disease in wild type and complement anaphylatoxin receptor-deficient mice (C3a receptor(-/-), C5a receptor(-/-) and C3aR(-/-)/C5aR(-/-)) and evaluated the eyes three weeks post-induction. No differences in disease severity or in disease incidence were seen between wild type controls and anaphylatoxin receptor-deficient mice. Our data indicate that C3a and C5a-mediated functions are not critical to the development of EAU.

摘要

为了确定补体过敏毒素介导致炎是否有助于实验性自身免疫性葡萄膜炎（EAU）的发展和进展，我们在野生型和补体过敏毒素受体缺陷型小鼠（C3a 受体（-/-）、C5a 受体（-/-）和 C3aR（-/-）/C5aR（-/-））中诱导疾病，并在诱导后 3 周评估眼睛。在疾病严重程度或疾病发生率方面，野生型对照与过敏毒素受体缺陷型小鼠之间没有差异。我们的数据表明，C3a 和 C5a 介导的功能对 EAU 的发展不是至关重要的。