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Immunol."],"abstract":"<jats:sec><jats:title>Introduction<\/jats:title><jats:p>Inflammation is a major pathological feature of pulmonary arterial hypertension (PAH), particularly in the context of inflammatory conditions such as systemic sclerosis (SSc). The endothelin system and anti-endothelin A receptor (ET<jats:sub>A<\/jats:sub>) autoantibodies have been implicated in the pathogenesis of PAH, and endothelin receptor antagonists are routinely used treatments for PAH. However, immunological functions of the endothelin B receptor (ET<jats:sub>B<\/jats:sub>) remain obscure.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Serum levels of anti-ET<jats:sub>B<\/jats:sub> receptor autoantibodies were quantified in healthy donors and SSc patients with or without PAH. Age-dependent effects of overexpression of prepro-endothelin-1 or ET<jats:sub>B<\/jats:sub> deficiency on pulmonary inflammation and the cardiovascular system were studied in mice. Rescued ET<jats:sub>B<\/jats:sub>-deficient mice (ET<jats:sub>B<\/jats:sub><jats:sup>-\/-<\/jats:sup>) were used to prevent congenital Hirschsprung disease. The effects of pulmonary T-helper type 2 (Th2) inflammation on PAH-associated pathologies were analyzed in ET<jats:sub>B<\/jats:sub><jats:sup>-\/-<\/jats:sup> mice. Pulmonary vascular hemodynamics were investigated in isolated perfused mouse lungs. Hearts were assessed for right ventricular hypertrophy. Pulmonary inflammation and collagen deposition were assessed <jats:italic>via<\/jats:italic> lung microscopy and bronchoalveolar lavage fluid analyses.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Anti-ET<jats:sub>B<\/jats:sub> autoantibody levels were elevated in patients with PAH secondary to SSc. Both overexpression of prepro-endothelin-1 and rescued ET<jats:sub>B<\/jats:sub> deficiency led to pulmonary hypertension, pulmonary vascular hyperresponsiveness, and right ventricular hypertrophy with accompanying lymphocytic alveolitis. Marked perivascular lymphocytic infiltrates were exclusively found in ET<jats:sub>B<\/jats:sub><jats:sup>-\/-<\/jats:sup> mice. Following induction of pulmonary Th2 inflammation, PAH-associated pathologies and perivascular collagen deposition were aggravated in ET<jats:sub>B<\/jats:sub><jats:sup>-\/-<\/jats:sup> mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>This study provides evidence for an anti-inflammatory role of ET<jats:sub>B<\/jats:sub>. ET<jats:sub>B<\/jats:sub> seems to have protective effects on Th2-evoked pathologies of the cardiovascular system. Anti-ET<jats:sub>B<\/jats:sub> autoantibodies may modulate ET<jats:sub>B<\/jats:sub>-mediated immune homeostasis.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fimmu.2022.895501","type":"journal-article","created":{"date-parts":[[2022,6,9]],"date-time":"2022-06-09T04:22:29Z","timestamp":1654748549000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":21,"title":["Endothelin B Receptor Immunodynamics in Pulmonary Arterial Hypertension"],"prefix":"10.3389","volume":"13","author":[{"given":"Christoph","family":"Tabeling","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carla R.","family":"Gonz\u00e1lez 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