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Journal of Immunology Research
Volume 2017, Article ID 8913860, 12 pages
Review Article

Cervical Carcinogenesis and Immune Response Gene Polymorphisms: A Review

1Department of Pathology, Leiden University Medical Centre, Leiden, Netherlands
2Laboratory of Immunogenetics, Department of Medical Microbiology and Infection Control, VU University Medical Centre, Amsterdam, Netherlands
3Institute for Public Health Genomics, Department of Genetics and Cell Biology, School for Oncology and Developmental Biology (GROW), Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, Netherlands
4Centre for Gynaecological Oncology Amsterdam, Amsterdam, Netherlands

Correspondence should be addressed to Ekaterina S. Jordanova; ln.cmul@avonadroj.e

Received 30 July 2016; Revised 28 November 2016; Accepted 18 December 2016; Published 9 February 2017

Academic Editor: Margarete D. Bagatini

Copyright © 2017 Akash M. Mehta et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The local immune response is considered a key determinant in cervical carcinogenesis after persistent infection with oncogenic, high-risk human papillomavirus (HPV) infections. Genetic variation in various immune response genes has been shown to influence risk of developing cervical cancer, as well as progression and survival among cervical cancer patients. We reviewed the literature on associations of immunogenetic single nucleotide polymorphism, allele, genotype, and haplotype distributions with risk and progression of cervical cancer. Studies on HLA and KIR gene polymorphisms were excluded due to the abundance on literature on that subject. We show that multiple genes and loci are associated with variation in risk of cervical cancer. Rather than one single gene being responsible for cervical carcinogenesis, we postulate that variations in the different immune response genes lead to subtle differences in the effectiveness of the antiviral and antitumour immune responses, ultimately leading to differences in risk of developing cervical cancer and progressive disease after HPV infection.