{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,31]],"date-time":"2026-10-31T01:09:11Z","timestamp":1793408951502,"version":"4.5.0"},"reference-count":70,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2007,10,1]],"date-time":"2007-10-01T00:00:00Z","timestamp":1191196800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2007,10,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>In the murine model of Cryptococcus neoformans infection Th1 (IL-12\/IFN-\u03b3) and Th17 (IL-23\/IL-17) responses are associated with protection, whereas an IL-4-dependent Th2 response exacerbates disease. To investigate the role of the Th2 cytokine IL-13 during pulmonary infection with C. neoformans, IL-13-overexpressing transgenic (IL-13Tg+), IL-13-deficient (IL-13\u2212\/\u2212), and wild-type (WT) mice were infected intranasally. Susceptibility to C. neoformans infection was found when IL-13 was induced in WT mice or overproduced in IL-13Tg+ mice. Infected IL-13Tg+ mice had a reduced survival time and higher pulmonary fungal load as compared with WT mice. In contrast, infected IL-13\u2212\/\u2212 mice were resistant and 89% of these mice survived the entire period of the experiment. Ag-specific production of IL-13 by susceptible WT and IL-13Tg+ mice was associated with a significant type 2 cytokine shift but only minor changes in IFN-\u03b3 production. Consistent with enhanced type 2 cytokine production, high levels of serum IgE and low ratios of serum IgG2a\/IgG1 were detected in susceptible WT and IL-13Tg+ mice. Interestingly, expression of IL-13 by susceptible WT and IL-13Tg+ mice was associated with reduced IL-17 production. IL-13 was found to induce formation of alternatively activated macrophages expressing arginase-1, macrophage mannose receptor (CD206), and YM1. In addition, IL-13 production led to lung eosinophilia, goblet cell metaplasia and elevated mucus production, and enhanced airway hyperreactivity. This indicates that IL-13 contributes to fatal allergic inflammation during C. neoformans infection.<\/jats:p>","DOI":"10.4049\/jimmunol.179.8.5367","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T19:19:36Z","timestamp":1397848776000},"page":"5367-5377","source":"Crossref","is-referenced-by-count":245,"title":["IL-13 Induces Disease-Promoting Type 2 Cytokines, Alternatively Activated Macrophages and Allergic Inflammation during Pulmonary Infection of Mice with\n                    <i>Cryptococcus neoformans<\/i>"],"prefix":"10.1093","volume":"179","author":[{"given":"Uwe","family":"Mu\u0308ller","sequence":"first","affiliation":[{"name":"Institute of Immunology, College of Veterinary Medicine, University of Leipzig , Leipzig ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Werner","family":"Stenzel","sequence":"additional","affiliation":[{"name":"Institute of Neuropathology, Medical Faculty, University of Cologne , Cologne ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabriele","family":"Ko\u0308hler","sequence":"additional","affiliation":[{"name":"Gerhard Domagk Institute for Pathology, University of Mu\u0308nster , Mu\u0308nster ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christoph","family":"Werner","sequence":"additional","affiliation":[{"name":"Division of Allergy and Pulmonology, Department of Pediatrics, Martin-Luther-University , Halle-Wittenberg, Halle ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tobias","family":"Polte","sequence":"additional","affiliation":[{"name":"Division of Allergy and Pulmonology, Department of Pediatrics, Martin-Luther-University , Halle-Wittenberg, Halle ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gesine","family":"Hansen","sequence":"additional","affiliation":[{"name":"Division of Allergy and Pulmonology, Department of Pediatrics, Martin-Luther-University , Halle-Wittenberg, Halle ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole","family":"Schu\u0308tze","sequence":"additional","affiliation":[{"name":"Institute of Immunology, College of Veterinary Medicine, University of Leipzig , Leipzig ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Reinhard K","family":"Straubinger","sequence":"additional","affiliation":[{"name":"Institute of Immunology, College of Veterinary Medicine, University of Leipzig , Leipzig ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manfred","family":"Blessing","sequence":"additional","affiliation":[{"name":"Institute of Immunology, College of Veterinary Medicine, University of Leipzig , Leipzig ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew N J","family":"McKenzie","sequence":"additional","affiliation":[{"name":"Medical Research Council Laboratory of Molecular Biology , Cambridge ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank","family":"Brombacher","sequence":"additional","affiliation":[{"name":"Institute of Infectious Disease and Molecular Medicine, University of Cape Town , Cape Town ,","place":["South Africa"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gottfried","family":"Alber","sequence":"additional","affiliation":[{"name":"Institute of Immunology, College of Veterinary Medicine, University of Leipzig , Leipzig ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2007,10,15]]},"reference":[{"key":"2026012809261920600_R1","first-page":"507","volume-title":"Med. 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