Immune privilege and inflammation of the testis

Immune privilege and inflammation of the testis
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DOI:
10.1159/000087816
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发表时间:
2005-01-01
期刊:
IMMUNOLOGY OF GAMETES AND EMBRYO IMPLANTATION
影响因子:
--
通讯作者:
Meinhardt, A
Meinhardt, A
中科院分区:
其他
文献类型:
--
作者:
Schuppe, HC;Meinhardt, A

文献摘要

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在哺乳动物(包括人类)的正常、未受影响的睾丸中发现了大量的免疫细胞。位于间质区室中,它们与使睾丸成为免疫特权部位的机制有关,在该部位,生殖细胞受到保护免受自身免疫攻击,并且外来组织移植物可以存活很长一段时间。关于睾丸的正常发育和功能,促细胞因子和促细胞因子已被证明发挥重要的调节作用。然而,睾丸环境并不排除导致炎症反应和潜在损伤的免疫激活。在实验动物中,用睾丸组织主动免疫或过继转移特异性T淋巴细胞引起自身免疫性睾丸炎。在男性中,生殖道(包括睾丸)的感染和炎症被广泛认为是不孕症的重要病因。由于细菌或病毒感染引起的症状性睾丸炎被认为是罕见的,而不育男性中无症状睾丸炎症反应的患病率很高。尽管病变呈斑片状分布,但炎症与睾丸功能(即精子发生)的破坏有关。淋巴细胞浸润和伴随的曲细精管损伤的模式支持了涉及自身反应性T细胞活化的概念。
Immune cells are found in considerable numbers within the normal, unaffected testes of mammals, including humans. Located in the interstitial compartment, they are implicated in the mechanisms that make the testis an immunologically privileged site where germ cells are protected from autoimmune attack and foreign tissue grafts may survive for extended periods of time. With regard to normal development and function of the testis, both pro-and antiinflammatory cytokines have been shown to play an important regulatory role. The testicular environment, however, does not preclude immune activation resulting in inflammatory reactions and potential damage. In experimental animals, active immunization with testicular tissue or adoptive transfer of specific T lymphocytes causes autoimmune orchitis. In men, infection and inflammation of the reproductive tract including the testes are widely accepted as important etiological factors of infertility. Whereas symptomatic orchitis due to bacterial or viral infections is considered to be rare, a high prevalence of asymptomatic testicular inflammatory reactions could be demonstrated among infertile males. Despite the patchy distribution of the lesions, inflammation is associated with disruption of testicular function, ie spermatogenesis. The pattern of lymphocyte infiltration and concomitant damage of seminiferous tubules supports the concept that activation of autoreactive T cells is involved.