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In young and middle-aged mice, Aire
In young and middle-aged mice, Aire deficiency appeared to be protective as supported by the reduced β-gal+ epithelial cells and the enhanced thymic output. However, once the autoimmune phenotype was fully developed in aged Aire-deficient mice, their thymuses underwent accelerated involution. In comparison to the age-matched wildtype littermates, old Aire-deficient mice showed lower numbers of total thymocytes and recent thymic emigrants but more β-gal+ thymic epithelial cells. This phenomenon may partly be attributable to the increased number of activated Th1 cells homing to the thymus. This speculation was further supported by the enhanced thymic aging following repeated challenges with complete Freund’s adjuvant immunization. Taken together, the present study highlights a unique mechanism by which autoimmunity facilitates the senescence of thymic epithelial cells through returning Th1 cells.
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在年轻和中年小鼠中，由于减少的β-gal+上皮细胞和增强的胸腺输出，Aire缺乏症似乎具有保护作用。但是，一旦在老龄Aire缺陷小鼠中完全建立了自身免疫表型，它们的胸腺就会加速退化。与年龄匹配的野生型同窝仔相比，Aire缺陷型小鼠的胸腺总细胞和近代胸腺迁徙者数量较少，但β-gal+胸腺上皮细胞较多。这种现象可能部分归因于归巢于胸腺的激活Th1细胞数量增加。反复进行全面弗氏佐剂免疫后，胸腺衰老增强，进一步支持了这种推测。在一起
正在翻译中..
In young and middle-aged mice, Aire deficiency appeared to be protective as supported by the reduced β-gal+ epithelial cells and the enhanced thymic output. However, once the autoimmune phenotype was fully developed in aged Aire-deficient mice, their thymuses underwent accelerated involution. In comparison to the age-matched wildtype littermates, old Aire-deficient mice showed lower numbers of total thymocytes and recent thymic emigrants but more β-gal+ thymic epithelial cells. This phenomenon may partly be attributable to the increased number of activated Th1 cells homing to the thymus. This speculation was further supported by the enhanced thymic aging following repeated challenges with complete Freund’s adjuvant immunization. Taken together, the present study highlights a unique mechanism by which autoimmunity facilitates the senescence of thymic epithelial cells through returning Th1 cells.
正在翻译中..
在中青年小鼠中，Aire缺乏似乎具有保护作用，因为β-gal+上皮细胞减少，胸腺输出增加。然而，一旦自身免疫表型在老年Aire缺陷小鼠中得到充分发展，它们的胸腺就会加速退化。与年龄相匹配的野生型窝鼠相比，老年Aire缺陷小鼠胸腺细胞总数和近期胸腺移植物数量较少，但β-gal+胸腺上皮细胞增多。这种现象可能部分归因于胸腺中活跃的Th1细胞数量的增加。这一推测得到了完全弗氏佐剂免疫反复挑战后胸腺衰老的进一步支持。综上所述，本研究强调了自身免疫通过返回Th1细胞促进胸腺上皮细胞衰老的独特机制。<br>
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