Abstract:

Rang Zhen*, Cui Fan, Li Wei, Wang Youwei. *Department of Dermatology, Institute of Dermatovenereology, Sichuan Academy of Medical Sciences and Sichuan Provincial People′s Hospital, Chengdu 610031, China Corresponding author: Li Wei, Email: tiantiantama@sina.com 【Abstract】 Objective To compare the Dectin-1 signal transduction pathway and its function on dendritic cells between a female patient with recurrent vulvovaginal candidiasis （RVVC） and a healthy woman, and to explore the possible mechanism for VVC recurrence in this patient. Methods Venous blood samples were collected from a female patient with RVVC and a healthy woman. Then, monocytes were isolated from the blood samples, and were induced to differentiate into dendritic cells （DCs） in vitro. The obtained DCs were divided into three groups to be cultured alone, cocultured with Candida albicans or the combination of Candida albicans and anti-Dectin-1 antibodies for different durations. Flow cytometry was performed to determine the expression levels of CD83, CD86 and CD80 on DCs to evaluate the maturity of DCs, Western blot analysis to measure the protein expressions of Dectin-1, Syk and CARD9 in DCs, and enzyme-linked immunosorbent assay （ELISA） to determine the levels of interleukin （IL） -23, tumor necrosis factor α （TNF-α） and IL-12 in the culture supernatant of DCs. Results After co-culture with Candida albicans for 24 hours, the expressions of CD83, CD86 and CD80 were significantly inhibited on the patient-derived DCs compared with the control-derived DCs. Western blot analysis showed no significant differences in the expression of Dectin-1 between the control-and patient-derived DCs, but a decrease in the expressions of phosphorylated-Syk and CARD9 in the patient-derived DCs compared with the control-derived DCs after 2-hour coculture with Candida albicans. After co-culture with Candida albicans for 6 hours, the levels of IL-23, TNF-α and IL-12 were lower in the culture supernatant of patient-derived DCs than in that of control-derived DCs. Furthermore, the anti-Dectin antibody showed no inhibitory effects on the activation of the Syk-dependent signal transduction pathway in or the secretion of the above cytokines by the patient-derived DCs. Conclusion The Dectin-1 signal transduction pathway was abnormal in DCs from the patient with RVVC, which may decelerate the maturation of DCs, inhibit the secretion of IL-23, TNF-α and IL-12 by them, and finally result in a defect in natural mucosal immunity against Candida infection in the host.