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Reversal of inflammatory reprogramming by vasodilator agents in pulmonary hypertension.

ERJ Open Res

January 2025

Center for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung and Blood Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine and UPMC, Pittsburgh, PA, USA.

Background: Pulmonary arterial hypertension (PAH) is a deadly disease without effective non-invasive diagnostic and prognostic testing. It remains unclear whether vasodilators reverse inflammatory activation, a part of PAH pathogenesis. Single-cell profiling of inflammatory cells in blood could clarify these PAH mechanisms.

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Therapeutic doses of efzofitimod demonstrate efficacy in pulmonary sarcoidosis.

ERJ Open Res

January 2025

Division of Pulmonary and Critical Care Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.

Background: In a phase 1b/2a clinical trial of efzofitimod in patients with corticosteroid-requiring pulmonary sarcoidosis, treatment resulted in dose-dependent improvement in key end-points. We undertook a analysis pooling dose arms that achieved therapeutic concentrations of efzofitimod (Therapeutic group) those that did not (Subtherapeutic group).

Methods: Peripheral blood mononuclear cells incubated with tuberculin-coated beads were exposed to varying concentrations of efzofitimod in an assay to determine concentrations that inhibited granuloma formation.

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Introduction: Severe cutaneous adverse reactions (SCARs) are life-threatening and often linked to antiepileptic drugs (AEDs). Common types of SCARs include Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), and drug reaction with eosinophilia and systemic symptoms (DRESS). Immune-mediated mechanisms involving human leukocyte antigen () alleles have been implicated in the pathogenesis of this reaction.

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Thalassemia is a hematological disorder caused by mutations in the hemoglobin gene, often necessitating regular blood transfusions. These frequent transfusions exert continuous pressure on patients' immune systems. Despite extensive research on the hematological aspects of thalassemia, few studies have explored the immune status of these patients.

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