Abstract
The transcription factor FOXP3 is an essential marker of the development and activation of regulatory T cells (Tregs), which are cells specialized in the regulation and normal tolerance of the immune response. In the context of chronic viral liver diseases, Tregs participate in the maintenance of infections by promoting histopathological control and favor the immune escape of viral agents by suppressing the antiviral response. Single nucleotide polymorphisms (SNPs) may influence the function of FOXP3 in a number of pathological conditions. The present study sought to evaluate the influence of SNPs in the FOXP3 gene promoter region in patients with chronic viral liver diseases. Three SNPs (−3279C>A, −2383C>T, and −924A>G) were analyzed in groups of patients with chronic hepatitis C (CHC), active chronic hepatitis B (CHB-A), inactive chronic hepatitis B (CHB-I), and a healthy control group (CG) using real-time PCR. The frequencies of the polymorphic variants were compared between groups and correlated with liver histopathological characteristics and enzyme levels [i.e., alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transpeptidase (GGT)] obtained via biopsy and from the clinical records of the participating patients, respectively. For the −2338C>T SNP, no significant differences were found in the frequencies of variants between groups or in the histological findings. Significant associations between the polymorphisms and the CHB-I group were not established. The −3279C>A SNP was associated with altered viral loads (log10) and GGT levels in CHC patients with advanced stages of inflammatory activity and liver fibrosis. The −924A>G SNP was associated with altered viral loads (log10) and liver enzyme levels among CHB-A patients with milder inflammation and fibrosis. However, the frequencies of the −3279C>A and −924A>G polymorphisms were not directly associated with the histopathological profiles of the analyzed patients. These polymorphic variants may influence hepatic function in patients with chronic viral liver diseases but are not directly associated with the establishment of the degree of inflammatory activity and liver fibrosis.
Highlights
Previous studies have shown that a sustained helper T and cytotoxic T lymphocyte response is closely associated with the disease courses of hepatitis B and C infections and that these cells are crucial for successful infection control [1,2,3]
Eleven chronic hepatitis C (CHC) and eight active chronic hepatitis B carriers (CHB-A) patients were not submitted to biopsy considering the high risk procedure as the previous results of transient elastography (TE) indicated severe alterations in the hepatic parenchyma; these patients were classified according to the degree of fibrosis
We propose that subsequent studies evaluate the role of this polymorphism
Summary
Previous studies have shown that a sustained helper T and cytotoxic T lymphocyte response is closely associated with the disease courses of hepatitis B and C infections and that these cells are crucial for successful infection control [1,2,3]. The liver itself, which is constantly exposed to antigenic stimulation, has acquired specialized mechanisms and cells that mediate immunotolerance properties and prevent excessive activation of the immune response [10,11,12]. In this context, there is strong evidence for the involvement of a specialized set of cells called regulatory T cells (Tregs) in the regulation of both the liver immune response and tolerance [13]. In chronic hepatitis C infection, different Treg subpopulations protect the host against tissue damage, and these cells are correlated with the degree of hepatic inflammation [18]
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