Abstract
Pulmonary arterial hypertension (PAH) is a relatively rare disease, but, today, its incidence tends to increase. The severe course of the disease and poor patient survival rate make PAH a major diagnostic and therapeutic challenge. For this reason, a thorough understanding of the pathogenesis of the disease is essential to facilitate the development of more effective therapeutic targets. Research shows that the development of PAH is characterized by a number of abnormalities within the immune system that greatly affect the progression of the disease. In this review, we present key data on the regulated function of immune cells, released cytokines and immunoregulatory molecules in the development of PAH, to help improve diagnosis and targeted immunotherapy.
Highlights
Another way to explain the presence of immunosuppressive molecules on the surface of lymphocytes, may be the functional exhaustion of cells that play a regulatory role in Pulmonary arterial hypertension (PAH)
A number of clinical studies have shown that disorders of the immune system play an important role in the development and maintenance of PAH
Registered dysregulation at the level of immune cells, the cytokines they release and, the negative effects noticed due to the action of immunoregulatory molecules indicate the complexity of this problem
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Recorded by means of direct, invasive hemodynamic measurements [1] This condition may be a manifestation of many clinical situations, e.g., it is associated with the aggravation of the underlying disease (left ventricular failure, acquired heart defects and respiratory system diseases) to which the therapy was administered. In other cases (HIV infection, certain drugs and toxins, gene mutations and systemic diseases of connective tissue), we can only talk about factors in the development of arterial hypertension, as its severity is related to the advancement of changes in the pulmonary bed [2]. These cases are collectively known as “pulmonary arterial hypertension”. Pulmonary hypertension (PH) induced through hypoxia was found not eligible, since it is defined as PH classification group 3 and, is not equivalent to PAH
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