The present study was designed to investigate the association between a change in vaginal local immunity and human papilloma virus (HPV) infection outcome in patients with cervical lesions, through the study of the expression of vaginal local immune factors, interleukin (IL)-2, IL-10, secretory immunoglobulin A (sIgA) and IgG, in patients with different grades of cervical lesions and different degrees of cervical lesions caused by HPV infection prior to and following treatment.
The present work aimed to investigate the possible association between IL10 and TNFα promoter polymorphisms and HPV infection in the cervical carcinogenesis risk in women from Brazil.
The reduction of dominant Lactobacillus in the vagina, impairment of H<sub>2</sub>O<sub>2</sub> function, flora ratio imbalance, pathogen infections, reduction in IL-2/IL-10 ratio, and changes in SIgA and IgG levels could all be potential factors that influenced the pathogenicity of HPV infection and the occurrence and development of cervical lesions.
Therefore, this interplay between HPV and IL-10 creates a vicious cycle that could favor an immunosuppressive microenvironment in the cervix, facilitating the progression of a simple HPV infection to SIL or cervical cancer.
Therefore, we evaluated the influence of IL-10 c.-592C>A polymorphism in HPV infection and in IL-10 plasmatic/cervical levels in HPV infected and non-infected women.
The present study aims to find out the impact of IL-10 promoter polymorphisms at -1082A/G (rs1800896), -819C/T (rs1800872), and -592C/A (rs1800871) sites along with IL-10 production and HPV infection in the progression of cervical cancer.
Using High Resolution Melt analysis (HRM), we analyzed an SNP -1082A/G and -819C/T in interleukin-10 promoter region in 364 Brazilian women: 171 with cervical lesions and HPV infection, and 193 with normal cytological results and HPV-negative.
Using longitudinal predictive indicators (SE, SP, PPV, NPV), IL-10 expression was of no value in predicting (1) the outcomes of HR-HPV infections, or (2) the surrogate endpoints (incident CIN1+, CIN2+) of progressive disease.
The IL10 GCC haplotype has been associated with production of relatively high levels of interleukin (IL)-10, which could (a) inhibit cytokines such as IL-2, TNF-alpha, IL-4, IL-6, and IL-12 that are involved in the T(H)1-T(H)2 immunoregulation; (b) down-regulate expression of MHC class I and class II molecules; or (c) induce the transcription of early promoter of HPV, all potentially contributing to duration of HPV infection among immunosuppressed individuals.
The up-regulated secretion of IL-10 may inhibit immune responses against HPV infection in early cervical lesions, whereas up-regulated TNF-alpha and uncoordinated cytokine secretion (elevated both Th1 and Th2 cytokines) may reflect impaired or invalid responses in advanced stage lesions.