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Adenosine signaling plays a central role in fibroblast activation. We undertook this study to evaluate the therapeutic effects of adenosine depletion with <jats:styled-content style=\"fixed-case\">PEG<\/jats:styled-content>ylated adenosine deaminase (<jats:styled-content style=\"fixed-case\">PEG<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ADA<\/jats:styled-content>) in preclinical models of <jats:styled-content style=\"fixed-case\">SS<\/jats:styled-content>c.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The effects of <jats:styled-content style=\"fixed-case\">PEG<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ADA<\/jats:styled-content> on inflammation, vascular remodeling, and tissue fibrosis were analyzed in Fra\u20102 mice and in a B10.D2\u2192<jats:styled-content style=\"fixed-case\">BALB<\/jats:styled-content>\/c (H\u20102<jats:sup>d<\/jats:sup>) model of sclerodermatous chronic graft\u2010versus\u2010host disease (<jats:styled-content style=\"fixed-case\">GVHD<\/jats:styled-content>). The effects of <jats:styled-content style=\"fixed-case\">PEG<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ADA<\/jats:styled-content> were confirmed in vitro in a human full\u2010thickness skin model.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">PEG<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ADA<\/jats:styled-content> effectively inhibited myofibroblast differentiation and reduced pulmonary fibrosis by 34.3% (with decreased collagen expression) (<jats:italic>P<\/jats:italic> = 0.0079; n = 6), dermal fibrosis by 51.8% (<jats:italic>P<\/jats:italic> = 0.0006; n = 6), and intestinal fibrosis by 17.7% (<jats:italic>P<\/jats:italic> = 0.0228; n = 6) in Fra\u20102 mice. Antifibrotic effects of <jats:styled-content style=\"fixed-case\">PEG<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ADA<\/jats:styled-content> were also demonstrated in sclerodermatous chronic <jats:styled-content style=\"fixed-case\">GVHD<\/jats:styled-content> (reduced by 38.4%) (<jats:italic>P<\/jats:italic> = 0.0063; n = 8), and in a human full\u2010thickness skin model. <jats:styled-content style=\"fixed-case\">PEG<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ADA<\/jats:styled-content> treatment decreased inflammation and corrected the M2\/Th2\/group 2 innate lymphoid cell 2 bias. Moreover, <jats:styled-content style=\"fixed-case\">PEG<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ADA<\/jats:styled-content> inhibited proliferation of pulmonary vascular smooth muscle cells (reduced by 40.5%) (<jats:italic>P<\/jats:italic> &lt; 0.0001; n = 6), and prevented thickening of the vessel walls (reduced by 39.6%) (<jats:italic>P<\/jats:italic> = 0.0028; n = 6) and occlusions of pulmonary arteries (reduced by 63.9%) (<jats:italic>P<\/jats:italic> = 0.0147; n = 6). Treatment with <jats:styled-content style=\"fixed-case\">PEG<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ADA<\/jats:styled-content> inhibited apoptosis of microvascular endothelial cells (reduced by 65.4%) (<jats:italic>P<\/jats:italic> = 0.0001; n = 6) and blunted the capillary rarefication (reduced by 32.5%) (<jats:italic>P<\/jats:italic> = 0.0199; n = 6). <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> sequencing demonstrated that treatment with <jats:styled-content style=\"fixed-case\">PEG<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ADA<\/jats:styled-content> normalized multiple pathways related to fibrosis, vasculopathy, and inflammation in Fra\u20102 mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Treatment with <jats:styled-content style=\"fixed-case\">PEG<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ADA<\/jats:styled-content> ameliorates the 3 cardinal features of <jats:styled-content style=\"fixed-case\">SS<\/jats:styled-content>c in pharmacologically relevant and well\u2010tolerated doses. These findings may have direct translational implications, as <jats:styled-content style=\"fixed-case\">PEG<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ADA<\/jats:styled-content> has already been approved by the Food and Drug Administration for the treatment of patients with <jats:styled-content style=\"fixed-case\">ADA<\/jats:styled-content>\u2010deficient severe combined immunodeficiency disease.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.41259","type":"journal-article","created":{"date-parts":[[2020,3,17]],"date-time":"2020-03-17T13:15:27Z","timestamp":1584450927000},"page":"1385-1395","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Recombinant Adenosine Deaminase Ameliorates Inflammation, Vascular Disease, and Fibrosis in Preclinical Models of Systemic Sclerosis"],"prefix":"10.1002","volume":"72","author":[{"given":"Yun","family":"Zhang","sequence":"first","affiliation":[{"name":"University of Erlangen\u2010Nuremberg  Erlangen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8724-2835","authenticated-orcid":false,"given":"Honglin","family":"Zhu","sequence":"additional","affiliation":[{"name":"University of Erlangen\u2010Nuremberg, Erlangen, Germany, and Xiangya Hospital and Central South University  Changsha China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Florian","family":"Layritz","sequence":"additional","affiliation":[{"name":"University of Erlangen\u2010Nuremberg  Erlangen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui","family":"Luo","sequence":"additional","affiliation":[{"name":"Xiangya Hospital and Central South University  Changsha China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Wohlfahrt","sequence":"additional","affiliation":[{"name":"University of Erlangen\u2010Nuremberg  Erlangen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chih\u2010Wei","family":"Chen","sequence":"additional","affiliation":[{"name":"University of Erlangen\u2010Nuremberg  Erlangen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3881-2325","authenticated-orcid":false,"given":"Alina","family":"Soare","sequence":"additional","affiliation":[{"name":"University of Erlangen\u2010Nuremberg  Erlangen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christina","family":"Bergmann","sequence":"additional","affiliation":[{"name":"University of Erlangen\u2010Nuremberg  Erlangen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Ramming","sequence":"additional","affiliation":[{"name":"University of Erlangen\u2010Nuremberg  Erlangen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Florian","family":"Groeber","sequence":"additional","affiliation":[{"name":"Universit\u00e4tsklinikum W\u00fcrzburg and Fraunhofer Institute for Interfacial Engineering and Biotechnology  W\u00fcrzburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian","family":"Reuter","sequence":"additional","affiliation":[{"name":"Universit\u00e4tsklinikum W\u00fcrzburg and Fraunhofer Institute for Interfacial Engineering and Biotechnology  W\u00fcrzburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"GianFranco","family":"Fornasini","sequence":"additional","affiliation":[{"name":"Leadiant Biosciences, Inc.  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