Conclusion
The dysfunction of host's lymphocytes and activation of TLRs in PBMCs were the important mechanism in varicella-zoster virus induced herpes zoster. TLRs might be the core targets for the therapy drug development in treating HZ.
Methods
Peripheral blood samples from 31 HZ patients and 32 age-sex-matched healthy controls were collected and analyzed. The protein levels and gene levels of toll-like receptors (TLRs) were detected in peripheral blood mononuclear cells (PBMCs) by flow cytometry and quantitative real-time PCR. Further, the characteristics of T cell subsets and cytokines were detected via a cytometric bead array.
Purpose
Herpes zoster (HZ) is caused by the varicella-zoster virus (VZV), and 20% of healthy humans and 50% of people with immune dysfunction have a high probability of suffering from HZ. This study aimed to screen dynamic immune signatures and explore the potential mechanism during HZ progression. Patients and
Results
Compared to healthy controls, the mRNA levels of TLR2, TLR4, TLR7, and TLR9 mRNA in PBMCs were significantly increased in HZ patients. The protein level of TLR4 and TLR7 was significantly increased in HZ patients, but the levels of TLR2 and TLR9 were dramatically decreased. The CD3+ T cells were constant in HZ and healthy controls. CD4+ T cells were decreased in HZ patients, while CD8+ T cells were increased, resulting in an improved CD4+/CD8+ T cells ratio. Further, it was found that Th2 and Th17 were not changed, but the decreased Th1 and upregulated Treg cells were found in HZ. The Th1/Th2 and Th17/Treg ratios were significantly decreased. Last, the levels of IL-6, IL-10, and IFN-γ were significantly increased, but IL-2, IL-4, and IL-17A had no significant changes.