Abstract: Objective：To explore the role of TLR3 in HPV16 persistent infection and cervical lesions. Methods：Collected 157 cases HPV 16 infected patients whose liquid-base cervical cytology report is no intraepithelial lesion or malignancy（NILM）. After 6 months observation, among them, 40 cases were detected HPV16 persistent infection（persistent infection group）, and the other 107 cases turned to be negative （non-persistent infection group）, meanwhile selected 206 cases HPV 16 infected patients and split them with different stages of cervical lesions into three groups :group A contains 119 cases （chronic cervicitis 102 cases and CINⅠ 17 cases）; group B contains 66 cases （CINⅡ-Ⅲ 57 cases and carcinoma in situ 9 cases）; group C contains 21 cases （cervical carcinoma 21 cases）. The expression of DNA TLR3 and IFN-β were detected by PCR. The mutation of TLR3 recycled productions were detected by gene sequencing respectively. Results：The expression levels of TLR3, IFN-β in persistent infection group were lower than those in non-persistent infection group, and the differences were statistically significant（P＜0.05）. TLR3 was positively correlated with IFN-β, which has statistically significant（P＜0.001）. The expressions of TLR3, IFN-β in different cervical lesions groups: in group A, B and C, the expression levels of TLR3 group A was higher than group B and group C （P＜0.05）; the expression levels of group B was higher than group C（P＜0.05）. The expression levels of IFN-β group A was higher than group B and group C （P＜0.05）; the expression levels of group B was higher than group C （P＜0.05). In three groups TLR3 was positively correlated with IFN-β, which has statistically significant（all P＜0.001）. Conclusions：The low expression level of TLR3 leads to cervical local immune dysfunction by down-regulating the expression of IFN-β. The reduction of TLR3 expression is not only related with the cervical HPV 16 persistent infection but also plays an important role in regulating the occurrence and progression of cervical lesions and cervical cancer.

Key words: Uterine cervical neoplasms, Human papillomavirus 16, Infection, Toll-like receptor 3, Interferon-beta