Impairment of the NKT–STAT1–CXCL9 Axis Contributes to Vessel Fibrosis in Pulmonary Hypertension Caused by Lung Fibrosis

Pulmonary hypertension (PH) is a common, severe comorbidity in interstitial lung diseases such as pulmonary fibrosis (PF), and it has limited treatment options. Excessive vascular fibrosis and inflammation are often present in PH, but the underlying mechanisms are still poorly understood. To identify a novel functional link between natural killer T (NKT) cell activation and vascular fibrosis in PF-PH. The study results indicate that the absence of NKT cells impairs the STAT1–CXCL9–CXCR3 axis in PF-PH and that restoration of this axis by NKT cell activation may unravel a novel therapeutic strategy to target vascular fibrosis in interstitial lung disease.