Thymic stromal lymphopoietin (TSLP) is associated with fungal keratitis. This work aims to investigate whether TSLP can regulate T helper (Th) 17 and regulatory T cell (Treg) differentiation. We separated dendritic cells (DCs) from peripheral blood of healthy volunteers. DCs were treated with TSLP to activate DCs, and exosomes were obtained. CD⁺ T cells were incubated with exosomes from TSLP-treated DCs. We found that exosomes from TSLP-treated DCs notably promoted the proportions of Th17 cells and inhibited the proportions of Tregs in the CD4⁺ T cells. Moreover, exosomes from TSLP-treated DCs enhanced the expression of retinoid-related orphan receptor γt (RORγt) and interleukin 17 (IL-17), and repressed the expression of forkhead box protein P3 (Foxp3) and interleukin 10 (IL-10) in the CD4⁺ T cells. Furthermore, miR-21 was highly expressed in exosomes from TSLP-treated DCs. Exosomes from TSLP-treated miR-21-silenced DCs promoted Treg differentiation and suppressed Th17 differentiation. Smad7 up-regulation repressed Th17 differentiation and enhanced Treg differentiation, which was abolished by miR-21 overexpression. Smad7 overexpression rescued the effect of exosomes from TSLP-treated DCs on Th17/Treg differentiation. In conclusion, our article confirms that TSLP induces DCs to deliver miR-21 by secreting exosomes, and thus miR-21 regulates Th17/Treg differentiation by inhibiting Smad7. Thus, this work further reveals the biological role of miR-21 in fungal keratitis.

胸腺基质淋巴细胞生成素（TSLP）与真菌性角膜炎相关。这项工作旨在调查TSLP是否可以调节T辅助（Th）17和调节T细胞（Treg）分化。我们从健康志愿者的外周血中分离出树突状细胞（DC）。用TSLP处理DC以激活DC，并获得外泌体。CD ⁺ T细胞与来自TSLP处理的DC的外来体一起孵育。我们发现，TSLP处理的DC的外来体显着提高了Th17细胞的比例，并抑制了CD4 ⁺中Tregs的比例。T细胞。此外，TSLP处理的DC的外泌体增强类维生素A相关孤儿受体γt（RORγt）和白介素17（IL-17）的表达，并抑制叉头盒蛋白P3（Foxp3）和白介素10（IL-10）的表达。在CD4 ⁺T细胞。此外，miR-21在TSLP处理的DC的外泌体中高度表达。TSLP处理的miR-21沉默的DC的外泌体促进Treg分化并抑制Th17分化。Smad7上调抑制了Th17分化并增强了Treg分化，这被miR-21过表达所消除。Smad7过表达挽救了外来体从TSLP处理的DC中对Th17 / Treg分化的影响。总之，我们的文章证实TSLP通过分泌外泌体诱导DC传递miR-21，因此miR-21通过抑制Smad7来调节Th17 / Treg分化。因此，这项工作进一步揭示了miR-21在真菌性角膜炎中的生物学作用。