{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T05:56:16Z","timestamp":1791006976132,"version":"4.1.0"},"reference-count":39,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2002,5,1]],"date-time":"2002-05-01T00:00:00Z","timestamp":1020211200000},"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":[[2002,5,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Allergic asthma is an inflammatory disease of the airways characterized by eosinophilic inflammation and airway hyper-reactivity. Cytokines and chemokines specific for Th2-type inflammation predominate in asthma and in animal models of this disease. The role of Th1-type inflammatory mediators in asthma remains controversial. IFN-\u03b3-inducible protein 10 (IP-10; CXCL10) is an IFN-\u03b3-inducible chemokine that preferentially attracts activated Th1 lymphocytes. IP-10 is up-regulated in the airways of asthmatics, but its function in asthma is unclear. To investigate the role of IP-10 in allergic airway disease, we examined the expression of IP-10 in a murine model of asthma and the effects of overexpression and deletion of IP-10 in this model using IP-10-transgenic and IP-10-deficient mice. Our experiments demonstrate that IP-10 is up-regulated in the lung after allergen challenge. Mice that overexpress IP-10 in the lung exhibited significantly increased airway hyperreactivity, eosinophilia, IL-4 levels, and CD8+ lymphocyte recruitment compared with wild-type controls. In addition, there was an increase in the percentage of IL-4-secreting T lymphocytes in the lungs of IP-10-transgenic mice. In contrast, mice deficient in IP-10 demonstrated the opposite results compared with wild-type controls, with a significant reduction in these measures of Th2-type allergic airway inflammation. Our results demonstrate that IP-10, a Th1-type chemokine, is up-regulated in allergic pulmonary inflammation and that this contributes to the airway hyperreactivity and Th2-type inflammation seen in this model of asthma.<\/jats:p>","DOI":"10.4049\/jimmunol.168.10.5278","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T18:26:04Z","timestamp":1398018364000},"page":"5278-5286","source":"Crossref","is-referenced-by-count":173,"title":["IFN-\u03b3-Inducible Protein 10 (CXCL10) Contributes to Airway Hyperreactivity and Airway Inflammation in a Mouse Model of Asthma"],"prefix":"10.1093","volume":"168","author":[{"given":"Benjamin D","family":"Medoff","sequence":"first","affiliation":[{"name":"Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Harvard Medical School , Boston, MA 02114"},{"name":"Pulmonary and Critical Care Unit, Massachusetts General Hospital, Harvard Medical School , Boston, MA 02114"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alain","family":"Sauty","sequence":"additional","affiliation":[{"name":"Division of Allergology and Clinical Immunology, Centre Hospitalier Universitaire Vaudois , Lausanne ,","place":["Switzerland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew M","family":"Tager","sequence":"additional","affiliation":[{"name":"Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Harvard Medical School , Boston, MA 02114"},{"name":"Pulmonary and Critical Care Unit, Massachusetts General Hospital, Harvard Medical School , Boston, MA 02114"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James A","family":"Maclean","sequence":"additional","affiliation":[{"name":"Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Harvard Medical School , Boston, MA 02114"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R Neal","family":"Smith","sequence":"additional","affiliation":[{"name":"Department of Pathology, Massachusetts General Hospital, Harvard Medical School , Boston, MA 02114"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anuja","family":"Mathew","sequence":"additional","affiliation":[{"name":"Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Harvard Medical School , Boston, MA 02114"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer H","family":"Dufour","sequence":"additional","affiliation":[{"name":"Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Harvard Medical School , Boston, MA 02114"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew D","family":"Luster","sequence":"additional","affiliation":[{"name":"Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Harvard Medical School , Boston, MA 02114"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2002,5,15]]},"reference":[{"key":"2026020208193629000_R1","first-page":"399","volume-title":"J. 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