{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T18:57:40Z","timestamp":1791313060034,"version":"4.3.1"},"reference-count":80,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2013,6,15]],"date-time":"2013-06-15T00:00:00Z","timestamp":1371254400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2013,6,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Interleukin-22 (IL-22) has redundant, protective, or pathogenic functions during autoimmune, inflammatory, and infectious diseases. Here, we addressed the potential role of IL-22 in host defense and pathogenesis during lethal and sublethal respiratory H3N2 influenza A virus (IAV) infection. We show that IL-22, as well as factors associated with its production, are expressed in the lung tissue during the early phases of IAV infection. Our data indicate that retinoic acid receptor-related orphan receptor-\u03b3t (ROR\u03b3t)-positive \u03b1\u03b2 and \u03b3\u03b4 T cells, as well as innate lymphoid cells, expressed enhanced\n            <jats:italic>Il22<\/jats:italic>\n            transcripts as early as 2 days postinfection. During lethal or sublethal IAV infections, endogenous IL-22 played no role in the control of IAV replication and in the development of the IAV-specific CD8\n            <jats:sup>+<\/jats:sup>\n            T cell response. During lethal infection, where wild-type (WT) mice succumbed to severe pneumonia, the lack of IL-22 did not accelerate or delay IAV-associated pathogenesis and animal death. In stark contrast, during sublethal IAV infection, IL-22-deficient animals had enhanced lung injuries and showed a lower airway epithelial integrity relative to WT littermates. Of importance, the protective effect of endogenous IL-22 in pulmonary damages was associated with a more controlled secondary bacterial infection. Indeed, after challenge with\n            <jats:named-content content-type=\"genus-species\">Streptococcus pneumoniae<\/jats:named-content>\n            , IAV-experienced\n            <jats:italic>Il22<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            animals were more susceptible than WT controls in terms of survival rate and bacterial burden in the lungs. Together, IL-22 plays no major role during lethal influenza but is beneficial during sublethal H3N2 IAV infection, where it limits lung inflammation and subsequent bacterial superinfections.\n          <\/jats:p>","DOI":"10.1128\/jvi.02943-12","type":"journal-article","created":{"date-parts":[[2013,4,18]],"date-time":"2013-04-18T00:17:19Z","timestamp":1366244239000},"page":"6911-6924","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":161,"title":["Interleukin-22 Reduces Lung Inflammation during Influenza A Virus Infection and Protects against Secondary Bacterial Infection"],"prefix":"10.1128","volume":"87","author":[{"given":"Stoyan","family":"Ivanov","sequence":"first","affiliation":[{"name":"Institut Pasteur de Lille, Centre d'Infection et d'Immunit\u00e9 de Lille, Lille, France"},{"name":"Universit\u00e9 Lille Nord de France, Lille, France"},{"name":"Centre National de la Recherche Scientifique, UMR 8204, Lille, 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