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实验性自身免疫性睾丸炎作为免疫性男性不育的模型。

Experimental autoimmune orchitis as a model of immunological male infertility.

作者信息

Naito Munekazu, Terayama Hayato, Hirai Shuichi, Qu Ning, Lustig Livia, Itoh Masahiro

机构信息

Department of Anatomy, Tokyo Medical University, 6-1-1 Shinjuku, Tokyo 160-8402, Japan.

出版信息

Med Mol Morphol. 2012 Dec;45(4):185-9. doi: 10.1007/s00795-012-0587-2. Epub 2012 Dec 7.

Abstract

Clinically, 60-75% of male infertility cases are categorized as idiopathic spermatogenic disturbance. In previous studies of this condition, lymphocytic infiltration and immune deposits were present in several testis biopsy specimens, indicating that inflammatory or immunological factors contribute to the occurrence of the lesions. However, there is currently little evidence regarding immunological infertility in men. Previously, we established an immunological infertility model, experimental autoimmune orchitis (EAO), that can be induced in mice by two subcutaneous injections of viable syngeneic testicular germ cells without the use of any adjuvant. In this EAO model, lymphocytes surround the tubuli recti and then induce spermatogenic disturbance. In addition, after the active inflammation stage of this model, the seminiferous epithelium is damaged irreversibly, resembling the histopathology of human male idiopathic spermatogenic disturbance. In the majority of patients with testicular autoimmunity, there is a chronic and asymptomatic development of the inflammatory reaction. Therefore, this disease is very difficult to diagnose at the ongoing stage, and it is possible that the histopathology of idiopathic spermatogenic disturbance in the clinic is reported at the post-active inflammation stage of autoimmune orchitis. In this review, the histopathology of EAO before and after inflammation is discussed, comparing it with human orchitis.

摘要

临床上,60% - 75%的男性不育病例被归类为特发性生精障碍。在以往对这种病症的研究中,多个睾丸活检标本中存在淋巴细胞浸润和免疫沉积物,这表明炎症或免疫因素促成了病变的发生。然而,目前关于男性免疫性不育的证据很少。此前,我们建立了一种免疫性不育模型,即实验性自身免疫性睾丸炎(EAO),无需使用任何佐剂,通过两次皮下注射活的同基因睾丸生殖细胞即可在小鼠中诱导产生。在这个EAO模型中,淋巴细胞围绕直精小管,进而诱导生精障碍。此外,在该模型的活跃炎症阶段之后,生精上皮会受到不可逆的损伤,类似于人类男性特发性生精障碍的组织病理学表现。在大多数睾丸自身免疫患者中,炎症反应呈慢性且无症状发展。因此,这种疾病在进展阶段很难诊断,临床上特发性生精障碍的组织病理学报告有可能是在自身免疫性睾丸炎的活跃炎症后期。在这篇综述中,我们讨论了EAO炎症前后的组织病理学,并将其与人类睾丸炎进行比较。

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