Itoh M, De-Rooij D, Takeuchi Y
Department of Cell Biology, Medical School, University of Utrecht, The Netherlands.
J Anat. 1995 Dec;187 ( Pt 3)(Pt 3):671-9.
We previously established an experimental model for autoimmune inflammation of the testis in mice by active immunisation with viable syngeneic testicular germ cells without the use of adjuvants. In the present study, the mode of spread of the inflammation was investigated histologically to determine vulnerable sites for the inflammatory cell infiltration. The results showed that lymphocytic infiltration first appeared in the tunica albuginea adjacent to the tubuli recti and the rete testis. In the next stage, infiltration with lymphocytes, macrophages, polymorphonuclear leucocytes and plasma cells occurred around the tubuli recti and subsequently a mixture of these cells spread centrifugally to the peripheral interstitium of the testis with persistent involvement of the region of the tubuli recti and the tunica albuginea. In the final stage, the inflammatory cells invaded the tubules. However, even in cases with the most severe testicular inflammation, the interstitium in the rete testis region showed only slight inflammatory changes, and no inflammation was seen in the ductuli efferentes, the epididymis or the vas deferens.
我们之前通过用活的同基因睾丸生殖细胞进行主动免疫,在不使用佐剂的情况下建立了小鼠睾丸自身免疫性炎症的实验模型。在本研究中,通过组织学研究炎症的传播方式,以确定炎症细胞浸润的易损部位。结果显示,淋巴细胞浸润首先出现在与直精小管和睾丸网相邻的白膜。在下一阶段,直精小管周围出现淋巴细胞、巨噬细胞、多形核白细胞和浆细胞浸润,随后这些细胞的混合物离心性扩散至睾丸外周间质,直精小管区域和白膜持续受累。在最后阶段,炎症细胞侵入小管。然而,即使在睾丸炎症最严重的病例中,睾丸网区域的间质仅表现出轻微的炎症变化,在输出小管、附睾或输精管中未观察到炎症。