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Expression of coinhibitory receptors on T cells in the microenvironment of usual vulvar intraepithelial neoplasia is related to proinflammatory effector T cells and an increased recurrence-free survival.
常见外阴上皮内瘤变微环境中 T 细胞上共抑制受体的表达与促炎效应 T 细胞和无复发生存期增加有关。

摘要

Human papillomavirus-induced usual-type vulvar intraepithelial neoplasia (uVIN) are infiltrated by immune cells but apparently not cleared. A potential explanation for this is an impaired T cell effector function by an immunesuppressive milieu, coinfiltrating regulatory T cells or the expression of coinhibitory molecules. Here, the role of these potential inhibitory mechanisms was evaluated by a detailed immunohistochemical analysis of T cell infiltration in the context of FoxP3, Tbet, indoleamine 2,3-dioxygenase, programmed cell death 1, T cell immunoglobulin mucin 3 (TIM3), natural killer cell lectin-like receptor A (NKG2A) and galectins-1, -3 and -9. Paraffin-embedded tissues of primary uVIN lesions (n=43), recurrent uVIN lesions (n=20), vulvar carcinoma (n=21) and healthy vulvar tissue (n=26) were studied. We show that the vulva constitutes an area intensely surveyed by CD8+, CD4+, Tbet+ and regulatory T cell populations, parts of which express the examined coinhibitory molecules. In uVIN especially, the number of regulatory T cells and TIM3+ T cells increased. The expression of the coinhibitory markers TIM3 and NKG2A probably reflected a higher degree of T cell activation as a dense infiltration with stromal CD8+TIM3+ T cells and CD3+NKG2A+ T cells was related to the absence of recurrences and/or a prolonged recurrence-free survival. A dense coinfiltrate with regulatory T cells was negatively associated with the time to recurrence, most dominantly when the stromal CD8+TIM3+ infiltration was limited. This notion was sustained in vulvar carcinoma's where the numbers of regulatory T cells progressively increased to outnumber coinfiltrating CD8+TIM3+ T cells and CD3+NKG2A+ T cells.

译文

人乳头瘤病毒诱导的普通型外阴上皮内瘤变 (uVIN) 被免疫细胞浸润,但显然没有清除。对此的一个潜在解释是免疫抑制环境、共同浸润调节性 T 细胞或共同抑制分子的表达导致的 T 细胞效应功能受损。这里,这些潜在抑制机制的作用是通过在 FoxP3 、 Tbet 、吲哚胺 2,3-双加氧酶、程序性细胞死亡 1 、 T 细胞免疫球蛋白黏蛋白 3 (TIM3),自然杀伤细胞凝集素样受体 A (NKG2A) 和 galectins-1,-3 和-9。原发性 uVIN 病变 (n = 43) 、复发性 uVIN 病变 (n = 20) 、外阴癌 (n = 21) 和健康外阴组织 (n = 26) 的石蜡包埋组织被研究过。我们表明,外阴构成了一个由 CD8 、 CD4 、 Tbet 和调节性 T 细胞群体密切调查的区域,其中部分表达了检测到的共抑制分子。尤其是在 uVIN 中,调节性 T 细胞和 TIM3 T 细胞的数量增加。共抑制标记物 TIM3 和 NKG2A 的表达可能反映了较高程度的 T 细胞活化,因为基质 CD8 TIM3 T 细胞和 CD3 NKG2A T 细胞的密集浸润与复发的缺失有关。和/或延长的无复发生存期。与调节性 T 细胞的密集共同浸润与复发时间呈负相关,最明显的是当基质 CD8 TIM3 浸润受限时。这一概念在外阴癌中得以持续,在外阴癌中,调节性 T 细胞的数量逐渐增加,超过共浸润的 CD8 TIM3 T 细胞和 CD3 NKG2A T 细胞。

vulvar intraepithelial neoplasia

妇产 外阴病变 疾病
概述  :  

阴道上皮内瘤变(vulvar intraepithelial neoplasia,VAIN)是一种疾病,多见于60岁以上妇女,描述了以增生异常改变为特征的阴道恶性组织学发现。这种疾病很罕见,通常没有症状。在Papanicolaou测试(巴氏涂片)中可通过异常细胞的存在来检测VAIN。就像宫颈上皮内瘤变一样,VAIN分为三个阶段,VAIN 1、2和3。在VAIN 1中,阴道皮肤细胞厚度的三分之一异常,而在VAIN 3中,整个厚度受到影响。VAIN 3也称为原位癌或0期阴道

vulvar   ['vʌlvə] 

释    义    adj. 外阴的;会阴部的

例    句    All the history and symptom mounted to support the diagnosis of vulvar vestibulitis syndrome.根据患者临床表现和病史,符合女阴前庭炎综合征的诊断。

 

intraepithelial  英 ['ɪntrə,epɪ'θiːlɪəl] 

释    义    adj. 上皮内的

例    句    All women who present with lower genital tract intraepithelial lesions should be offered HIV testing because of the high incidence of neoplasia in this population. 所有的有生殖道低度上皮内病变的妇女需检查HIV,因为在这一人群中发病率较高。

 

neoplasia  英 [,niːə(ʊ)'pleɪzɪə]  美 [,nio'pleʒɪr] 

释    义    n. 瘤形成

例    句    Thus, cells respond to regular growth control, differentiating the process from neoplasia. 因此,细胞是受正常生长调控的,不同于肿瘤的形成。

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