S100, CD68, and MHC class II molecule expression in cervical high- and low-grade HPV-induced lesions

• Published in: Revista da Sociedade Brasileira de Medicina Tropical Vol. 45; no. 1; pp. 3 - 8
• Main Authors: Cassandri, Fernanda, Apardecia Tozetti, Ines, dos Santos Fernandes, Carlos Eurico, Gatto de Almeida, Flavia, Ribeiro Falcao, Gustavo, Lins Scapulatempo, Ilzia Doraci, Martins Prata, Thago Theodoro, Junqueira Padovani, Cacilda Tezelli, Borges Alves, Daniella, Teixeira Ferreira, Alda, Auxiliadora Gomes Sandim Abdo, Maria
• Format: Journal Article
• Language: English
• Published: 01.01.2012
• Subjects: Human papillomavirus
• DOI: 10.1590/S0037-8682201200010000
• ISSN: 0037-8682

INTRODUCTION: Some human papillomavirus (HPV) types are involved in malignant processes in the cervical epithelium, with 99% of cases attributed to oncogenic HPV infection. This study aimed to detect S100, CD68, and major histocompatibility complex class II (MHC-II) molecules in cervical uterine epithelial samples in patients with high- and low-grade lesions induced by HPV. METHODS: Fifty-eight samples from patients who were confirmed positive or negative for high-risk oncogenic HPV DNA, had histopathological diagnosis of cervical intraepithelial neoplasia (CIN) of grades I, II, or III, or were negative for intraepithelial lesion or malignancy were subjected to immunohistochemistry reaction to S100 protein, CD68, and MHC-II (HLA-DR alpha chain). RESULTS: The presence of MHC-II predominated in samples exhibiting histopathological alterations (p < 0.05). S100 detection was more numerous in carcinoma samples (CIN III) (75%). Presence of this protein correlated significantly (p < 0.05) with histopathological findings and viral load. CONCLUSIONS: A small expression of CD68 was observed, which may be explained by the observation in our study having been made on random microscopic fields and not on specific areas. The findings, such as the presence of S100 protein and MHC-II expression in samples with histological alterations, could suggest that the immune system fails to control HPV replication at the early stages of infection. Further studies with larger prospective data are necessary to confirm this result.