Chaberek Katarzyna, Mrowiec Martyna, Kaczmarek Magdalena, Dutsch-Wicherek Magdalena
2nd Department of Obstetrics and Gynaecology, Center of Postgraduate Medical Education (CMKP), 01-813 Warsaw, Poland.
Department of Endoscopic Otorhinolaryngology, Center of Postgraduate Medical Education (CMKP), 01-813 Warsaw, Poland.
Diagnostics (Basel). 2022 Aug 6;12(8):1906. doi: 10.3390/diagnostics12081906.
The development of malignancy is closely connected with the process of cancer microenvironment remodeling. As a malignancy develops, it stimulates the creation of the suppressive microenvironment of the tumor through the presence of cells that express membrane proteins. These proteins are secreted into the cancer microenvironment, where they enable tumor growth. In patients with cancer of the cervix, the development of the disease is also linked to high-risk HPV (hr-HPV) infection. Such infections are common, and most clear spontaneously; however, a small percentage of these infections can persist and progress into precancerous cervical intraepithelial neoplasia and invasive cervical carcinoma. Consequently, it is assumed that the presence of hr-HPV infection alone is not sufficient for the development of cancer. However, chronic HPV infection is associated with the induction of the remodeling of the microenvironment of the epithelium. Furthermore, the local microenvironment is recognized as a cofactor that participates in the persistence of the HPV infection and disease progression. This review presents the selected immune evasion mechanisms responsible for the persistence of HPV infection, beginning with the delay in the virus replication process prior to the maturation of keratinocytes, the shift to the suppressive microenvironment by a change in keratinocyte immunomodulating properties, the alteration of the Th1/Th2 polarization of the immune response in the microenvironment, and, finally, the role of HLA-G antigen expression.
恶性肿瘤的发展与癌症微环境重塑过程密切相关。随着恶性肿瘤的发展，它通过表达膜蛋白的细胞的存在刺激肿瘤抑制性微环境的形成。这些蛋白被分泌到癌症微环境中，在那里它们促进肿瘤生长。在宫颈癌患者中，疾病的发展也与高危型人乳头瘤病毒（hr-HPV）感染有关。这种感染很常见，大多数会自发清除；然而，这些感染中有一小部分可能会持续存在并发展为癌前宫颈上皮内瘤变和浸润性宫颈癌。因此，人们认为仅存在hr-HPV感染不足以引发癌症。然而，慢性HPV感染与上皮微环境重塑的诱导有关。此外，局部微环境被认为是参与HPV感染持续存在和疾病进展的一个辅助因素。本综述介绍了导致HPV感染持续存在的特定免疫逃逸机制，首先是角质形成细胞成熟前病毒复制过程的延迟，通过角质形成细胞免疫调节特性的改变向抑制性微环境的转变，微环境中免疫反应的Th1/Th2极化的改变，以及最后HLA-G抗原表达的作用。
