LAUSR

Pulmonary hypertension (PH) is a life-threatening pathological state with elevated pulmonary arterial pressure, resulting in right ventricular failure and heart functional failure. Analyses of human samples and rodent models of pH support the infiltration of various immune cells, including neutrophils, mast cells, dendritic cells, B-cells, T-cells, and natural killer cells, to the lungs and pulmonary perivascular regions and their involvement in the PH development. There is evidence that macrophages are presented in the pulmonary lesions of pH patients as first-line myeloid leucocytes. Macrophage accumulation and presence, both M1 and M2 phenotypes, is a distinctive hallmark of pH which plays a pivotal role in pulmonary artery remodeling through various cellular and molecular interactions and mechanisms, including CCL2 and CX3CL1 chemokines, adventitial fibroblasts, glucocorticoid-regulated kinase 1 (SGK1), crosstalk with other immune cells, leukotriene B4 (LTB4), bone morphogenetic protein receptor 2 (BMPR2), macrophage migration inhibitory factor (MIF), and thrombospondin-1 (TSP-1). In this paper, we reviewed the molecular mechanisms and the role of immune cells and responses are involved in PH development. We also summarized the polarization of macrophages in response to different stimuli and their pathological role and their infiltration in the lung of pH patients and animal models.