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为探讨IL17A是否与缺氧性肺动脉高压(PH)的发生发展有关，将C57B6野生型(WT)和IL17A缺陷型(KO)小鼠暴露于低压低氧(HEMO)中长达42天。低氧21d后，WT/HEMO组大鼠右室收缩压(RVSP)、右室肥厚(RVH)程度及肌化外周血管百分比(%肌肉化)均高于WT对照组。KO/HEMO组和WT/HEMO组RVSP、RVH差异无统计学意义。KO/HEMO组与WT/HEMO组相比，肌力百分比略有下降。在PH形成过程中，WT/HEMO组炎性细胞因子升高，而KO/HEMO组较WT/HEMO组抗炎细胞因子升高。综上所述，IL17A可能与缺氧性PH的进展有关，然而，需要进一步的研究才能阐明。

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.