皮肤性病诊疗学杂志2026，Vol.33Issue(4)：243-252,10.DOI:10.3969/j.issn.1674-8468.2026.04.001
雌二醇通过抑制JAK/STAT介导的炎症反应并重塑T细胞表型促进复发性外阴阴道念珠菌病的发病
Estradiol promotes the pathogenesis of recurrent vulvovaginal candidiasis by suppressing jak/stat-mediated inflammation and remodeling T cell phenotypes
摘要
Abstract
Objective To explore the effects of estradiol(E2)on the expression of epithelial cell inflammatory cytokines(IL-17/IL-36 family),as well as on JAK/STAT phosphorylation and phenotypic differentiation of T cells.Methods C.albicans infection models were established using VK2/E6E7 cells and human CD4+naïve T lymphocytes,respectively.Both models were divided into four groups:a control group,an E2 group(containing 10-8 mol/L E2),a C.albicans group(containing 1 × 106 cfu/mL C.albicans),and a C.albicans+E2 group(containing 10-8 mol/L E2 and 1 × 106 cfu/mL C.albicans).In the VK2/E6E7 cell model,the expression levels of mR-NA for inflammatory cytokines,including IL-17A,IL-17F,IL-36α,IL-36β,and IL-36γ,were detected by RT-qPCR,while protein levels were measured by ELISA.In the CD4+naïve T lym-phocyte model,the phosphorylation levels of JAK(1-3)and STAT(1-3)were detected by Western blot,and the expression levels of T cell phenotypic markers,such as CD45R0,CD69,and CD103,were analyzed by flow cytometry.Results In C.albicans-infected VK2/E6E7 cells,the expression levels of pro-inflammatory cytokines(IL-17A,IL-17F,IL-36α,IL-36β,and IL-36γ)were significantly upregulated compared to the control group(P＜0.01).In contrast,the E2+C.albicans group significantly downregulated expression of these cytokines compared to the C.albi-cans group(P＜0.01).In human CD4+naïve T cells,phosphorylation levels of JAK(1-2)and STAT(1-2)were significantly increased in the C.albicans group compared to the control group(P＜0.05),and were significantly decreased in the E2+C.albicans group compared to the C.al-bicans group(P＜0.05),while no significant changes were observed for JAK3 and STAT3(P＞0.05).Additionally,the E2 group showed significant downregulation of CD45RO and CD69 ex-pression(P＜0.001)and significant upregulation of CD103 expression(P＜0.001)compared to the control group.Conclusions E2 downregulates the expression levels of pro-inflammatory cyto-kines(IL-17A,IL-17F,IL-36 α,IL-36β,IL-36γ)in C.albicans-infected vaginal epithelial cells and inhibits C.albicans-induced phosphorylation of JAK(1-2),STAT(1-2)in human CD4+naïve T lymphocytes.By inhibiting the JAK/STAT signaling pathway,E2 reshapes the activation and tissue-residency phenotypes of CD4+T cells,thereby impairing local antifungal immune clear-ance and promoting the pathogenesis of recurrent vulvovaginal candidiasis.关键词
复发性外阴阴道念珠菌病/白念珠菌/雌二醇/炎症因子/JAK/STAT通路/CD4+初始T淋巴细胞Key words
recurrent vulvovaginal candidiasis/Candida albicans/estradiol/inflammato-ry cytokines/JAK/STAT signaling pathway/CD4+naïve T lymphocytes引用本文复制引用
李恺欣,魏娜,李思齐,钟莉,刘蔚,梁小爽,林映萍,陈嵘祎..雌二醇通过抑制JAK/STAT介导的炎症反应并重塑T细胞表型促进复发性外阴阴道念珠菌病的发病[J].皮肤性病诊疗学杂志,2026,33(4):243-252,10.基金项目
东莞市社会科技发展重点项目(20221800905452) （20221800905452）
南方医科大学皮肤病教改课题(ZP202401) （ZP202401）
