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为了研究IL17A是否与缺氧诱导的肺动脉高压（PH）的发展有关，C57B6野生型（WT）和IL17A缺陷（KO）小鼠暴露于低压缺氧（hypo）长达42天。缺氧21 d后，WT/低氧组大鼠右心室收缩压（RVSP）、右心室肥厚（RVH）程度、周围血管肌肉化百分比（%肌肉化百分比）均较WT对照组升高。KO/ hypoo组与WT/ hypoo组RVSP、RVH无显著差异。与WT/ hypoo组相比，KO/ hypoo组肌肉百分率略有下降。与WT/ hypoo组相比，WT/ hypoo组在PH发育过程中炎症因子增加，KO/ hypoo组抗炎因子增加。总之，IL17A可能与缺氧PH的进展有关，但需要进一步的研究来阐明。

To investigate whether IL17A is associated with the development of hypoxia-induced pulmonary hypertension (PH), C57B6 wild type (WT) and IL17A-deficient (KO) mice were exposed to hypobaric hypoxia (hypo) for up to 42 days. The degreeof right ventricle systolic pressure (RVSP) and right ventricular hypertrophy (RVH), and percentages of muscularized peripheral vessels (%muscularity) were increased in WT/hypo group compared with WT control group after 21-day hypoxia. No difference was observed in RVSP, RVH between KO/hypo and WT/hypo group. There was slight decrease in %muscularity in KO/hypo group compared with that in WT/hypo group. Inflammatory cytokines were increased in the development process of PH in WT/hypo group, whereas, anti-inflammatory cytokines were increased in KO/hypo group compared with WT/hypo group. In conclusion, IL17A might be associated with the progression of hypoxic PH, however, additional studies are necessary in order to be elucidated.