Immunological prevention of age-related hearing loss : analysis of its molecular biological mechanisms

我们发现，通过接种年轻的CD4^+T细胞或胎儿胸腺移植来恢复受者免疫，导致CD4^+T细胞中白细胞介素1受体II(IL-1R2)基因的下调，并减少SAMP1小鼠(人类衰老的小鼠模型)与年龄相关的听力损失。我们对年龄相关性全身免疫功能障碍与神经退变机制之间关系的研究为治疗神经衰老开辟了新的途径，包括老年性耳聋，目前尚无有效的治疗方法。

We found that rejuvenation of the recipient immunity by inoculation of young CD4^+T cells or a fetal thymus graft led to down regulation of the interleukin 1 receptor type II(IL-1R2) gene in CD4^+T cells and reduced age-related hearing loss in SAMP1 mice, a murine model of human senescence. Our studies on the relationship between age-related systemic immune dysfunctions and neurodegeneration mechanisms open up new avenues of treatment of neurosenescence, including presbycusis, for which there is no effective therapy.