{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T11:54:37Z","timestamp":1779191677809,"version":"3.51.4"},"reference-count":35,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2013,3,1]],"date-time":"2013-03-01T00:00:00Z","timestamp":1362096000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Allergy"],"published-print":{"date-parts":[[2013,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Extracellular Adenosine\u20105\u2032\u2010Triphosphate (<jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>) is known to accumulate in the lung, following allergen challenge, and contributes via activation of purinergic receptors on dendritic cells (<jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>), to the development of allergic airway inflammation (<jats:styled-content style=\"fixed-case\">AAI<\/jats:styled-content>). Extracellular <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content> levels in the airways are normally tightly regulated by <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>39. This ectonucleotidase is highly expressed by <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content> purified from skin (Langerhans cells) and bone marrow, and has been shown to modulate <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content> adaptive\/haptenic immune responses. In this study, we have evaluated the impact of Cd39 deletion and associated perturbation of purinergic signaling in <jats:styled-content style=\"fixed-case\">AAI<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Standard ovalbumin (<jats:styled-content style=\"fixed-case\">OVA<\/jats:styled-content>)\u2013alum and house dust mite (<jats:styled-content style=\"fixed-case\">HDM<\/jats:styled-content>) bone marrow\u2010derived <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">BMDC<\/jats:styled-content>)\u2010dependent models of <jats:styled-content style=\"fixed-case\">AAI<\/jats:styled-content> were used to study effects of Cd39. Migration assays, time lapse microscopy, and T\u2010cell priming assays were further used to determine functional relevance of Cd39 expression on <jats:styled-content style=\"fixed-case\">BMDC<\/jats:styled-content> in the setting of immune and Th2\u2010mediated responses in these models.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:italic>Cd39<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice exhibited marked increases in <jats:styled-content style=\"fixed-case\">BALF ATP<\/jats:styled-content> levels but paradoxically exhibited limited <jats:styled-content style=\"fixed-case\">AAI<\/jats:styled-content> in both <jats:styled-content style=\"fixed-case\">OVA<\/jats:styled-content>\u2013alum and <jats:styled-content style=\"fixed-case\">HDM<\/jats:styled-content> models. These pathophysiological abnormalities were associated with decreased myeloid <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content> activation and chemotaxis toward <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>, and were linked to purinergic receptor desensitization responses. Further, <jats:italic>Cd39<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s exhibited limited capacity to both prime Th2 responses and form stable immune synaptic interactions with <jats:styled-content style=\"fixed-case\">OVA<\/jats:styled-content>\u2010transgenic na\u00efve T cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p><jats:italic>Cd39<\/jats:italic>\u2010deficient <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s exhibit limited capacity to induce Th2 immunity in a <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>\u2010driven model of <jats:styled-content style=\"fixed-case\">AAI <\/jats:styled-content><jats:italic>in vivo<\/jats:italic>. Our data demonstrate a role of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>39 and perturbed purinergic signaling in models of <jats:styled-content style=\"fixed-case\">AAI<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/all.12119","type":"journal-article","created":{"date-parts":[[2013,3,2]],"date-time":"2013-03-02T05:30:13Z","timestamp":1362202213000},"page":"472-480","source":"Crossref","is-referenced-by-count":25,"title":["Attenuated allergic airway inflammation in <i>Cd39<\/i> null mice"],"prefix":"10.1111","volume":"68","author":[{"given":"M.","family":"Idzko","sequence":"first","affiliation":[{"name":"Department of Pneumology University Medical Center"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C.","family":"K. Ayata","sequence":"additional","affiliation":[{"name":"Department of Pneumology University Medical Center"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T.","family":"M\u00fcller","sequence":"additional","affiliation":[{"name":"Department of Pneumology University Medical Center"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T.","family":"D\u00fcrk","sequence":"additional","affiliation":[{"name":"Department of Pneumology University Medical Center"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Grimm","sequence":"additional","affiliation":[{"name":"Department of Pneumology University Medical Center"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Baudi\u00df","sequence":"additional","affiliation":[{"name":"Department of Pneumology University Medical Center"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R. P.","family":"Vieira","sequence":"additional","affiliation":[{"name":"Department of Pneumology University Medical Center"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Cicko","sequence":"additional","affiliation":[{"name":"Department of Pneumology University Medical Center"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C.","family":"Boehlke","sequence":"additional","affiliation":[{"name":"Department of Nephrology University Medical Center Freiburg Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"Zech","sequence":"additional","affiliation":[{"name":"Department of Pneumology University Medical Center"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Sorichter","sequence":"additional","affiliation":[{"name":"Department of Pneumology University Medical Center"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Pelletier","sequence":"additional","affiliation":[{"name":"Centre de recherche en Rhumatologie et Immunologie Centre Hospitalier Universitaire de Qu\u00e9bec"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"S\u00e9vigny","sequence":"additional","affiliation":[{"name":"Centre de recherche en Rhumatologie et Immunologie Centre Hospitalier Universitaire de Qu\u00e9bec"},{"name":"D\u00e9partement de microbiologie\u2010infectiologie et d'immunologie Facult\u00e9 de M\u00e9decine Universit\u00e9 Laval Qu\u00e9bec QC Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S. 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