Department of Pathology, University of Virginia, Charlottesville, VA 22908, USA.
J Reprod Immunol. 2013 Nov;100(1):66-75. doi: 10.1016/j.jri.2013.08.004. Epub 2013 Sep 8.
CD4+ CD25+ regulatory T cells (Tregs) strongly influence the early and late autoimmune responses to meiotic germ cell antigens (MGCA) and the gonadal immunopathology in vasectomized mice. This is supported by the published and recently acquired information presented here. Within 24h of unilateral vasectomy (uni-vx) the ipsilateral epididymis undergoes epithelial cell apoptosis followed by necrosis, severe inflammation, and granuloma formation. Unexpectedly, vasectomy alone induced MGCA-specific tolerance. In contrast, uni-vx plus simultaneous Treg depletion resulted in MGCA-specific autoimmune response and bilateral autoimmune orchitis. Both tolerance and autoimmunity were strictly linked to the early epididymal injury. We now discovered that testicular autoimmunity in uni-vx mice did not occur when Treg depletion was delayed by one week. Remarkably, this delayed Treg depletion also prevented tolerance induction. Therefore, tolerance depends on a rapid de novo Treg response to MGCA exposed after vasectomy. Moreover, tolerance was blunted in mice genetically deficient in PD-1 ligand, suggesting the involvement of induced Treg. We conclude that pre-existing natural Treg prevents post-vasectomy autoimmunity, whereas vasectomy-induced Treg maintains post-vasectomy tolerance. We further discovered that vasectomized mice were still resistant to autoimmune orchitis induction for at least 12-16 months; thus, tolerance is long-lasting. Although significant sperm autoantibodies of low titers became detectable in uni-vx mice at 7 months, the antibody titers fluctuated over time, suggesting a dynamic "balance" between the autoimmune and tolerance states. Finally, we observed severe epididymal fibrosis and hypo-spermatogenesis at 12 months after uni-vx: findings of highly critical clinical significance.
CD4+ CD25+ 调节性 T 细胞(Tregs)强烈影响对减数分裂生殖细胞抗原(MGCA)的早期和晚期自身免疫反应以及输精管结扎小鼠的性腺免疫病理学。这得到了这里呈现的已发表和最近获得的信息的支持。在单侧输精管结扎术(uni-vx)后 24 小时内,同侧附睾经历上皮细胞凋亡,随后发生坏死、严重炎症和肉芽肿形成。出乎意料的是,单纯输精管结扎术即可诱导 MGCA 特异性耐受。相比之下,uni-vx 加同时 Treg 耗竭导致 MGCA 特异性自身免疫反应和双侧自身免疫性睾丸炎。耐受和自身免疫均严格与早期附睾损伤相关。我们现在发现,当 Treg 耗竭延迟一周时,uni-vx 小鼠的睾丸自身免疫并未发生。值得注意的是,这种延迟的 Treg 耗竭也阻止了耐受诱导。因此,耐受取决于对输精管结扎术后暴露的 MGCA 的快速新产生的 Treg 反应。此外,在 PD-1 配体基因缺失的小鼠中,耐受减弱,表明诱导的 Treg 参与其中。我们得出结论,预先存在的天然 Treg 可防止输精管结扎术后的自身免疫,而输精管结扎术诱导的 Treg 则维持输精管结扎术后的耐受。我们还发现,至少在 12-16 个月内,输精管结扎的小鼠仍然对自身免疫性睾丸炎的诱导具有抗性;因此,耐受是持久的。尽管在 uni-vx 小鼠中在 7 个月时可检测到低滴度的显著精子自身抗体,但抗体滴度随时间波动,表明自身免疫和耐受状态之间存在动态“平衡”。最后,我们观察到 uni-vx 后 12 个月附睾严重纤维化和少精子症:这是具有高度临床重要性的发现。