School of Medicine, Federal University of Juiz de Fora, Belo Horizonte, Minas Gerais, Brazil.
Int J Gynecol Cancer. 2012 Oct;22(8):1291-6. doi: 10.1097/IGC.0b013e318263ef88.
Local immunity plays an important role in the cervical defense mechanisms that prevent the development of cervical intraepithelial neoplasia. The objective of this study was to determine the involvement of local immunity by evaluating Langerhans cell (LC) density in cervical biopsies of human immunodeficiency virus (HIV)-positive and HIV-negative women.
A cross-sectional study was developed by including HIV-positive and HIV-negative women. All patients presented human papillomavirus DNA from the uterine cervix, which was detected by polymerase chain reaction or hybrid capture II. Cervical biopsies were assessed for LC density and cervical intraepithelial neoplasia. Langerhans cells were identified by immunohistochemistry using anti-CD1a and anti-S100 antibodies. Associations among cervical LC density, the type of cervical lesion, CD4 lymphocyte count, and HIV viral load were analyzed using logistic regression (SPSS, version 12.0).
Seventy-seven women (40 seropositive and 37 seronegative) were enrolled. The mean ± SD LC density identified with the anti-CD1a antibody was 0.80 ± 0.7 cells versus 2.6 ± 1.6 cells (P < 0.0001), whereas the mean ± SD LC density identified by the anti-S100 antibody was 1.3 ± 1.0 cells versus 3.6 ± 1.7 cells (P < 0.0001) among the HIV-positive and HIV-negative women, respectively. There were no associations between LC density and HIV viral load, CD4 lymphocyte count, or human papillomavirus genotype (P > 0.05). In a logistic regression model, HIV infection was the only factor independently associated with a decrease in LC density.
Human immunodeficiency virus infection was found to be an independent factor that explains the decrease in local immunity in the uterine cervix, which could allow the development of cervical lesions. This effect was not associated with CD4 lymphocyte count or HIV viral load.
局部免疫在防止宫颈上皮内瘤变发展的宫颈防御机制中起着重要作用。本研究旨在通过评估人类免疫缺陷病毒（HIV）阳性和 HIV 阴性妇女宫颈活检中的朗格汉斯细胞（LC）密度，来确定局部免疫的参与情况。
通过纳入 HIV 阳性和 HIV 阴性妇女进行了一项横断面研究。所有患者均有人乳头状瘤病毒（HPV）DNA 从子宫颈呈阳性，这是通过聚合酶链反应或杂交捕获 II 检测到的。宫颈活检评估 LC 密度和宫颈上皮内瘤变。通过使用抗 CD1a 和抗 S100 抗体的免疫组织化学鉴定朗格汉斯细胞。使用逻辑回归（SPSS 版本 12.0）分析 LC 密度与宫颈病变类型、CD4 淋巴细胞计数和 HIV 病毒载量之间的相关性。
共纳入 77 名女性（40 名血清阳性和 37 名血清阴性）。用抗 CD1a 抗体鉴定的平均 ± SD LC 密度为 0.80 ± 0.7 个细胞，而 HIV 阳性和 HIV 阴性妇女的抗 S100 抗体鉴定的平均 ± SD LC 密度分别为 2.6 ± 1.6 个细胞（P <0.0001）。LC 密度与 HIV 病毒载量、CD4 淋巴细胞计数或 HPV 基因型之间均无相关性（P >0.05）。在逻辑回归模型中，HIV 感染是唯一与 LC 密度降低独立相关的因素。
HIV 感染被认为是导致子宫颈局部免疫降低的独立因素，这可能导致宫颈病变的发生。这种影响与 CD4 淋巴细胞计数或 HIV 病毒载量无关。
