Lustig L, Doncel G F, Berensztein E, Puig R P, Denduchis B
Medicina (B Aires). 1989;49(3):225-31.
Experimental autoimmune orchitis (EAO) has been extensively studied in spite of which its pathogenic mechanisms are still poorly understood. It has been mostly induced in guinea pigs using spermatozoa or a testicular homogenate plus adjuvants. Initially, the aim of our work was to establish if non-spermatic antigens, such as extracellular components of the walls of seminiferous tubules, were able to induce an autoimmune orchitis. For this purpose, we obtained from rat testes: a) a preparation rich in basement membranes of seminiferous tubules (STBM) and b) a soluble fraction of STBM, non-related to collagen (D-STBM), presenting common antigenic determinants with laminin, the main non-collagen glycoprotein of basement membranes. Fifty per cent of rats immunized with STBM, D-STBM or a murine laminin, developed a multifocal and moderate damage of the testes characterized by mild interstitial cell infiltrates, alterations of the basement membranes of seminiferous tubules and Sertoli cells, sloughing of the germinal epithelium and tubular atrophy. Circulating antibodies and a specific cellular immune response were also detected. Moreover, rats passively injected with an heterologous anti-D-STBM serum developed a similar testicular lesion and showed Ig deposits on the basement membranes of seminiferous tubules. In relation to the pathogenic mechanisms of EAO, we studied the variations of T and B cell populations, at the immunization draining lymph nodes, during the development of orchitis. A severe EAO was induced in Wistar rats by immunization with an homologous testes homogenate plus adjuvants.(ABSTRACT TRUNCATED AT 250 WORDS)
尽管实验性自身免疫性睾丸炎(EAO)已得到广泛研究,但其致病机制仍知之甚少。它大多是在豚鼠身上通过使用精子或睾丸匀浆加佐剂诱导产生的。最初,我们研究的目的是确定非精子抗原,如曲细精管管壁的细胞外成分,是否能够诱发自身免疫性睾丸炎。为此,我们从大鼠睾丸中获取了:a)富含曲细精管基底膜的制剂(STBM),以及b)与胶原蛋白无关的STBM可溶性部分(D - STBM),它与层粘连蛋白具有共同抗原决定簇,层粘连蛋白是基底膜的主要非胶原蛋白糖蛋白。用STBM、D - STBM或鼠层粘连蛋白免疫的大鼠中,50%出现了睾丸多灶性中度损伤,其特征为轻度间质细胞浸润、曲细精管基底膜和支持细胞改变、生精上皮脱落以及小管萎缩。还检测到了循环抗体和特异性细胞免疫反应。此外,被动注射异源抗D - STBM血清的大鼠出现了类似的睾丸病变,并在曲细精管基底膜上显示有免疫球蛋白沉积。关于EAO的致病机制,我们研究了睾丸炎发展过程中免疫引流淋巴结处T和B细胞群体的变化。通过用同源睾丸匀浆加佐剂免疫Wistar大鼠诱导出了严重的EAO。(摘要截取自250字)