CD4(+) T细胞的转移会加重免疫缺陷的载脂蛋白E基因敲除小鼠的动脉粥样硬化。
Transfer of CD4(+) T cells aggravates atherosclerosis in immunodeficient apolipoprotein E knockout mice.
作者信息
Zhou X, Nicoletti A, Elhage R, Hansson G K
机构信息
Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
出版信息
Circulation. 2000 Dec 12;102(24):2919-22. doi: 10.1161/01.cir.102.24.2919.
BACKGROUND
Atherosclerosis is associated with immune responses to oxidized lipoproteins and certain microorganisms, but the role of specific immunity has remained unclear.
METHODS AND RESULTS
To study the role of immunity in atherosclerosis, we crossed atherosclerosis-prone apoE(-/-) mice with immunodeficient scid/scid mice. The offspring showed a 73% reduction in aortic fatty streak lesions when compared with immunocompetent apoE(-/-) mice. Transfer of CD4(+) T cells from apoE(-/-) to immunodeficient apoE(-/-)/scid/scid mice increased lesions by 164%. This was associated with the infiltration of transferred T cells into lesions, increased circulating interferon-gamma levels, and increased I-A expression in lesions.
CONCLUSIONS
CD4(+) T cells carry disease-promoting immunity in atherosclerosis.
背景
动脉粥样硬化与对氧化脂蛋白和某些微生物的免疫反应相关，但特异性免疫的作用仍不清楚。
方法与结果
为研究免疫在动脉粥样硬化中的作用，我们将易患动脉粥样硬化的载脂蛋白E基因敲除（apoE(-/-)）小鼠与免疫缺陷的严重联合免疫缺陷（scid/scid）小鼠进行杂交。与具有免疫能力的apoE(-/-)小鼠相比，后代小鼠主动脉脂肪条纹病变减少了73%。将apoE(-/-)小鼠的CD4(+) T细胞转移到免疫缺陷的apoE(-/-)/scid/scid小鼠中，病变增加了164%。这与转移的T细胞浸润到病变中、循环干扰素-γ水平升高以及病变中I-A表达增加有关。
结论
CD4(+) T细胞在动脉粥样硬化中携带促进疾病的免疫作用。
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