Fetal thymus graft enables recovery from age-related hearing loss and expansion of CD4-Positive T cells expressing IL-1 receptor type 2 and regulatory T Cells.
Fetal thymus graft enables recovery from age-related hearing loss and expansion of CD4-Positive T cells expressing IL-1 receptor type 2 and regulatory T Cells.
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DOI：
10.1186/s12979-015-0053-9
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Inaba M
中科院分区：
文献类型：
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作者：
Iwai H;Inaba M
越来越多的证据表明系统性免疫系统与包括内耳在内的中枢神经系统之间的关系。我们已经证明，在6个月大的小鼠中观察到的与年龄相关的T细胞功能障碍、听力损失和耳蜗螺旋神经节（SG）神经元变性的发展在12个月大的小鼠中得到恢复，这些小鼠先前接受了两次胎儿胸腺移植。我们还证明，表达白细胞介素1受体2型（IL-1 R2）的CD 4 + T细胞和天然存在的调节性T细胞（nT细胞），在12个月大的小鼠中扩增，在相同年龄的胸腺移植小鼠中减少。可以想象，通过胎儿胸腺移植物恢复全身免疫功能不仅有助于细胞免疫的激活，而且还有助于IL-1 R2 + CD 4 + T细胞或nT细胞的减少，这些细胞加速年龄相关性听力损失（阿勒）和耳蜗神经元的神经变性。应设计进一步研究IL-1 R2在CD 4 + T细胞、THL和神经元细胞上的表达之间的相互作用，以及胎儿胸腺移植和全身免疫恢复之间的关系，以促进对神经衰老（包括阿勒）的治疗作用。
Accumulating evidence has indicated the relationship between the systemic immune system and the central nervous system including the inner ear. We have shown that age-related developments of T-cell dysfunction, hearing loss, and degeneration of cochlear spiral ganglion (SG) neurons observed in 6-month-old mice were recovered in 12 months old mice which previously given fetal thymus transplants twice. We have also demonstrated that CD4+ T cells expressing interleukin 1 receptor type 2 (IL-1R2) and naturally occurring regulatory T cells (nTregs), which expanded in aged 12-month-old mice, were reduced in the thymus-grafted mice of the same age. It is conceivable that the rejuvenation of systemic immune function by fetal thymus grafts contributes not only to the activation of cellular immunity but also to the decrease of IL-1R2+ CD4+ T cells or nTregs, which cells accelerate both age-related hearing loss (AHL) and neurodegeneration of the cochlear neurons. Further studies on the interactions among IL-1R2 expression on CD4+ T cells, Tregs, and neuronal cells and also on the relationships between fetal thymus grafting and the rejuvenation of systemic immunity should be designed in order to advance towards therapeutic effects on neurosenescence, including AHL.