诱导型一氧化氮合酶缺陷的小鼠易患实验性自身免疫性葡萄膜视网膜炎。
Mice deficient in inducible nitric oxide synthase are susceptible to experimental autoimmune uveoretinitis.
作者信息
Silver P B, Tarrant T K, Chan C C, Wiggert B, Caspi R R
机构信息
Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
出版信息
Invest Ophthalmol Vis Sci. 1999 May;40(6):1280-4.
PURPOSE
Nitric oxide (NO) is an important mediator of inflammatory tissue damage. The present study addresses the question whether inducible nitric oxide synthase (iNOS), and consequently the ability to upregulate NO, is required to effect the pathogenesis of experimental autoimmune uveoretinitis (EAU) in mice.
METHODS
Mice with a homologous disruption of the iNOS gene (iNOS KO) were evaluated for their ability to develop EAU and associated cellular responses after immunization with the interphotoreceptor retinoid-binding protein. EAU was determined by histopathology 21 days after uveitogenic immunization, and antigen-specific cellular responses were assessed by delayed type hypersensitivity and lymphocyte proliferation.
RESULTS
iNOS knockout (iNOS KO) mice developed EAU with scores similar to wild-type mice and exhibited good cellular responses to the immunizing antigen.
CONCLUSIONS
A functional iNOS gene is not necessary for EAU pathogenesis. Therefore, upregulation of NO is not required to mediate autoimmune tissue damage in the eye.
目的
一氧化氮（NO）是炎症组织损伤的重要介质。本研究探讨了诱导型一氧化氮合酶（iNOS）以及上调NO的能力是否是小鼠实验性自身免疫性葡萄膜视网膜炎（EAU）发病机制所必需的。
方法
用视网膜间视黄醇结合蛋白免疫后，评估诱导型一氧化氮合酶基因同源性缺失的小鼠（iNOS基因敲除小鼠，iNOS KO）发生EAU的能力及相关细胞反应。在致葡萄膜炎免疫后21天通过组织病理学确定EAU，并通过迟发型超敏反应和淋巴细胞增殖评估抗原特异性细胞反应。
结果
iNOS基因敲除（iNOS KO）小鼠发生EAU的评分与野生型小鼠相似，并对免疫抗原表现出良好的细胞反应。
结论
功能性iNOS基因对于EAU发病机制并非必需。因此，介导眼部自身免疫组织损伤不需要上调NO。
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