Abstract
ObjectiveTo explore the molecular immune mechanism of HPV‐infected HaCaT cells in vitro based on TLRs signaling pathway by analyzing the effects of interfering TLRs on inflammatory and immune factors in the signaling pathway.MethodsFCM was used to analyze the proportion of Th1, Th2, Th17, and Treg cells in blood samples. HPV‐infected HaCaT cells were divided into five groups: A, B, C, D, and E. Group A added TLR3 antagonist, group B added TLR9 antagonist, group C added equivalent saline, group D added IRF3 agonist, and group E added IRF3 inhibitor. Immunohistochemistry was used to analyze the expression of TLR3 and TLR9 in HaCaT cell model; ELISA was used to analyze the expression of inflammatory factors IL‐2, TNF‐a, and IFN‐beta; WB was used to analyze the expression of TRAF3, IKK epsilon, and TBK1; RT‐PCR was used to analyze the expression of IRF3 and IRF7 in each cell model.ResultsThe proportion of blood immune cells in patients with HPV infection was Th1, Th17, Th2, and Treg, with statistical significance (P < .05); the expression of TLR3 and TLR9 in HPV‐infected cells was higher than that in negative control group, with statistical significance (P < .05); TLR3 was higher than TLR9, with no significant difference (P > .05); the expression of IL‐2, TNF‐alpha, IFN‐beta in each group, TLR3, and TLR9 was higher than that in negative control group (P < .05). The expression of TRAF3, IKK epsilon, and TBK1 in the control group was higher than that in the TLR3 and TLR9 inhibitor groups, and the expression of IRF3 and IRF7 in the TLR9 inhibitor group was higher than that in the TLR3 inhibitor group (P < .05); the expression of IRF3 and IRF7 in the TLR3i and TLR9i inhibitor groups was lower than that in the TLR3 inhibitor group (P < .05). Compared with the control group, IRF3a group was higher than the control group, IRF3i group was lower than the control group, the difference was statistically significant (P < .05).ConclusionTLR3 and TLR9, the key factors of TLRs, are highly expressed in HaCaT cells infected with HPV. Through TLRs‐IKK‐e‐IRFs‐IFN signaling pathway, they can induce high expression of inflammatory factors, IKK‐e, IRFs, and IFN, and improve immunity.
Highlights
Human papillomavims (HPV) is a class of non-enveloped DNA viruses with strict host range and tissue specificity
The expression of Toll-like receptors (TLRs) signaling pathway-related factors, immune factors, and inflammatory factors in HaCaT cells infected with HPV was determined to explore the molecular immune mechanism of HPV-infected HaCaT cells in vitro based on TLRs signaling pathway
Group A was treated with polyinosinic acidpolycytidylic acid (PIC), group B was treated with CpG oligonucleotide, group C was treated with saline, group D was treated with IRF3 agonist, and group E was treated with IRF3 inhibitor
Summary
Human papillomavims (HPV) is a class of non-enveloped DNA viruses with strict host range and tissue specificity. The treatment is not difficult, but the recurrence rate is high, and the incidence is increasing year by year.[1,2] It has been suggested that the expression of TLR3 and TLR9, the typical factors of Toll-like receptors (TLRs), is related to the clearance of HPV16 virus, but the mechanism is still unclear.[3] TLRs are a family of transmembrane signal transduction receptors that mediate innate immunity. They can recognize the conservative molecular components of specific microorganisms, that is pathogen-related molecular patterns, and resist the invasion of foreign pathogenic microorganisms.[4] TLR3 and TLR9 are considered as one of the important receptors of antiviral immunity. The expressions of TLR3 and TLR9 in HaCaT cell models were analyzed by immunohistochemistry
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
