My research interest is the pathogenetic mechanisms underlying various forms of pulmonary hypertension (PH). We described that arterial and chronic thromboembolic PH share pathogenetic mechanisms by showing comparable acute vasoreactivity. Based on these findings we successfully introduced vasodilator therapy in many patients with chronic thromboembolic PH. We found that patients with idiopathic PH have increased regulatory and decreased cytotoxic T cells in their blood and that their B lymphocytes express a different RNA pattern compared with healthy controls. Our results support a pathogenetic role of the immune system in PH. We demonstrated that sleep related breathing disorders, osteoporosis and hyperparathyroidism are common in PH and found that genetic polymorphism of the serotonin transporter are associated with PH in COPD. Some of these findings may have important implication for the management and treatment of PH-patients.