ArticleBMC immunology2011
Indispensable roles of OX40L-derived signal and epistatic genetic effect in immune-mediated pathogenesis of spontaneous pulmonary hypertension.
Article in BMC immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Plasma GDF-15 and PSP-D Predict the Development of Pulmonary Arterial Hypertension in Systemic Sclerosis.Pulmonary circulation · 2026Article
- OX40 (CD134) Expression on T Regulatory Cells Is Related to Serious Hypertensive Disorders in Pregnancy.Journal of cardiovascular development and disease · 2023Article
- TNF superfamily control of tissue remodeling and fibrosis.Frontiers in immunology · 2023Review
- Expression of CD70 Modulates Nitric Oxide and Redox Status in Endothelial Cells.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Myeloid-Derived Suppressor Cells and Pulmonary Hypertension.International journal of molecular sciences · 2018Review
- Targeting Costimulatory Pathways in Systemic Sclerosis.Frontiers in immunology · 2018Review
- B cell OX40L supports T follicular helper cell development and contributes to SLE pathogenesis.Annals of the rheumatic diseases · 2017Article
- Pulmonary endothelial cell DNA methylation signature in pulmonary arterial hypertension.Oncotarget · 2017Article
- OX40L blockade protects against inflammation-driven fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Regulatory T cells in cardiovascular diseases.Nature reviews. Cardiology · 2016Review
- Inflammation and immunity in the pathogenesis of pulmonary arterial hypertension.Circulation research · 2014Review
- A brief overview of mouse models of pulmonary arterial hypertension: problems and prospects.American journal of physiology. Lung cellular and molecular physiology · 2012Review
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPulmonary hypertension (PH) refers to a spectrum of diseases with elevated pulmonary artery pressure. Pulmonary arterial hypertension (PAH) is a disease category that clinically presents with severe PH and that is histopathologically characterized by the occlusion of pulmonary arterioles, medial muscular hypertrophy, and/or intimal fibrosis. PAH occurs with a secondary as well as a primary onset. Secondary PAH is known to be complicated with immunological disorders. The aim of the present study is to histopathologically and genetically characterize a new animal model of PAH and clarify the role of OX40 ligand in the pathogenesis of PAH.
resultsSpontaneous onset of PAH was stably identified in mice with immune abnormality because of overexpression of the tumor necrosis factor (TNF) family molecule OX40 ligand (OX40L). Histopathological and physical examinations revealed the onset of PAH-like disorders in the C57BL/6 (B6) strain of OX40L transgenic mice (B6.TgL). Comparative analysis performed using different strains of transgenic mice showed that this onset depends on the presence of OX40L in the B6 genetic background. Genetic analyses demonstrated a susceptibility locus of a B6 allele to this onset on chromosome 5. Immunological analyses revealed that the excessive OX40 signals in TgL mice attenuates expansion of regulatory T cells the B6 genetic background, suggesting an impact of the B6 genetic background on the differentiation of regulatory T cells.
conclusionPresent findings suggest a role for the OX40L-derived immune response and epistatic genetic effect in immune-mediated pathogenesis of PAH.
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