ArticleJournal of clinical laboratory analysis2020
Molecular immune mechanisms of HPV-infected HaCaT cells in vitro based on toll-like receptors signaling pathway.
Article in Journal of clinical laboratory analysis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Interferon Gamma and Secretory Immunoglobulin A Levels Decrease in Persistent Anal Condyloma Acuminatum Infection.Annals of dermatology · 2025Article
- Peptide GTSFTTTAER FromFood science & nutrition · 2025Article
- HPV infection status among women of all ages in Jinshan District, Shanghai.The Journal of international medical research · 2024Article
- Human papillomavirus associated cervical lesion: pathogenesis and therapeutic interventions.MedComm · 2023Review
- Exosomes: A potential tool for immunotherapy of ovarian cancer.Frontiers in immunology · 2022Review
- Molecular immune mechanisms of HPV-infected HaCaT cells in vitro based on toll-like receptors signaling pathway.Journal of clinical laboratory analysis · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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