Gonçalves M A G, Soares E G, Fernandes A P M, Fonseca B A L, Bettini J S R, Simões R T S, Donadi E A
Division of Clinical Immunology, Department of Medicine, School of Medicine of Ribeirão Preto, University of São Paulo, Av. Bandeirantes, 3900, 14049-900 Ribeirão Preto, São Paulo, Brazil.
Eur J Obstet Gynecol Reprod Biol. 2004 Jun 15;114(2):221-7. doi: 10.1016/j.ejogrb.2003.10.026.
The progression of immunosuppression in human immunodeficiency virus (HIV)+ women has been correlated with elevated incidence of squamous intraepithelial lesions (SIL), probably indicating the role of local immune milieu. In this study, we analysed S100, and HLA class II molecule expression in cervical biopsies according to HIV status, to the severity of SIL and to human papillomavirus (HPV) type.
Biopsies from 34 HIV+ and 44 HIV- patients with normal cervix or low- or high-grade SIL were studied. Langerhans' cells (LC) (S100), HLA class II and HLA-DQ molecules were evaluated by immunohistochemistry. HPV detection was performed using polymerase chain reaction (PCR). For statistical analysis Mann-Whitney (P< or =0.05) and Spearman test were used.
Epithelial S100 and HLA class II density were significantly increased with the severity of lesion (P=0.032; P=0.005). Epithelial S100+ increased in HPV+ (P=0.038), and HLA class II density decreased in HPV 16+ (P=0.035) or 18+ (P<0.0001) samples. HIV infection was associated with increased stromal S100+ (P=0.0005) and decreased HLA class II densities (P=0.0001). Decreased stromal S100+ was observed in women with CD4<500 cells/microl (P=0.050). Among HIV+ patients with SIL, the lowest S100 and epithelial HLA class II densities were detected in women with CD4<200 cells/microl (P=0.045).
After the establishment of AIDS, increased numbers of immature LCs and a reduction in HLA class II occurred, possibly turning the cervical milieu more favourable to HPV persistence. HPV 16 and 18 infections may interfere with the antigen presenting activity, possibly as an evasion mechanism.
人类免疫缺陷病毒(HIV)阳性女性免疫抑制的进展与鳞状上皮内病变(SIL)发病率升高相关,这可能表明局部免疫环境的作用。在本研究中,我们根据HIV状态、SIL严重程度和人乳头瘤病毒(HPV)类型,分析了宫颈活检组织中S100和HLA II类分子的表达。
研究了34例HIV阳性和44例HIV阴性的宫颈正常或低级别或高级别SIL患者的活检组织。通过免疫组织化学评估朗格汉斯细胞(LC)(S100)、HLA II类和HLA - DQ分子。使用聚合酶链反应(PCR)进行HPV检测。统计分析采用曼 - 惠特尼检验(P≤0.05)和斯皮尔曼检验。
上皮S100和HLA II类密度随病变严重程度显著增加(P = 0.032;P = 0.005)。HPV阳性样本中上皮S100 +增加(P = 0.038),HPV 16阳性(P = 0.035)或18阳性(P < 0.0001)样本中HLA II类密度降低。HIV感染与基质S100 +增加(P = 0.0005)和HLA II类密度降低(P = 0.0001)相关。CD4<500个细胞/微升的女性中观察到基质S100 +减少(P = 0.050)。在患有SIL的HIV阳性患者中,CD4<200个细胞/微升的女性中检测到最低的S100和上皮HLA II类密度(P = 0.045)。
艾滋病确立后,未成熟LC数量增加且HLA II类减少,这可能使宫颈环境更有利于HPV持续存在。HPV 16和18感染可能干扰抗原呈递活性,这可能是一种逃避机制。