Immune concept of human papillomaviruses and related antigens in local cancer milieu of human cervical neoplasia
Journal
Journal of Obstetrics and Gynaecology Research
Journal Volume
33
Journal Issue
2
Pages
103-113
Date Issued
2007
Author(s)
Abstract
It is presently the right time for clarifying human papillomavirus (HPV)-associated cellular immunity and clinical implications before global HPV vaccination programs begin. Infection with oncogenic HPV associates with the progression of cervical neoplasia. Both cellular and humoral immune responses are essential for the clearance of HPV-associated cervical lesions. There is increasing evidence that the immune system plays a pivotal role in determining the outcome of HPV infection. Viruses and associated neoplastic cells are proposed to have evolved mechanisms to avoid immune attack. T-cell-mediated immune responses against oncogenic HPV are believed to play a central role in cervical carcinogenesis. The presence of HPV-specific cytotoxic T lymphocytes (CTL) in a majority of human cervical cancer patients provides an approach for further study of their functional role in modulating this malignancy. Tumor-infiltrating lymphocytes (TIL) develop as manifestations of the recognition and defense against malignant cells by the host immune system. Cancer cells may overcome immune surveillance, either by downregulating the proliferation of HPV-specific CTL, or altering the effector compositions of immune cells against HPV infections. TIL in the tumor microenvironment can be functionally inhibited and lose the ability of clonal proliferation as a result of depressed expression of IL-2Rα. The upregulation of inhibitory signaling relates to the modulation of the virus- and/or tumor-specific immune responses. Alteration of host genetic susceptibility may also lead to abnormal immune response as a general genomic instability resulting from virus persistence. Induction of HPV-specific immune responses is anticipated as an intimate point for the treatment of cervical neoplasia. ? 2007 The Authors.
SDGs
Other Subjects
HLA antigen; interleukin 2 receptor alpha; protein E6; protein E7; Wart virus vaccine; cancer cell; cancer patient; carcinogenesis; cell proliferation; cellular immunity; clinical trial; cytotoxic T lymphocyte; cytotoxicity; dendritic cell; down regulation; genetic susceptibility; genomic instability; health program; human; humoral immunity; immune response; immune system; immunocompetent cell; immunosurveillance; microenvironment; nonhuman; outcome assessment; persistent virus infection; protein expression; review; signal transduction; T lymphocyte; tumor associated leukocyte; tumor cell; tumor growth; tumor virus; upregulation; uterine cervix cancer; uterine cervix carcinoma; uterine cervix carcinoma in situ; uterine cervix disease; uterine cervix tumor; vaccination; virus infection; Wart virus; Antigens, Viral; Dendritic Cells; Epitopes, T-Lymphocyte; Female; Genetic Predisposition to Disease; Humans; Immunity, Cellular; Lymphocytes, Tumor-Infiltrating; Oncogene Proteins; Papillomavirus Infections; T-Lymphocytes; Uterine Cervical Neoplasms
Type
review