{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T13:50:59Z","timestamp":1792158659922,"version":"4.4.0"},"reference-count":70,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2002,4,1]],"date-time":"2002-04-01T00:00:00Z","timestamp":1017619200000},"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":[[2002,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>IFN-\u03b3-inducible protein 10 (IP-10, CXCL10), a chemokine secreted from cells stimulated with type I and II IFNs and LPS, is a chemoattractant for activated T cells. Expression of IP-10 is seen in many Th1-type inflammatory diseases, where it is thought to play an important role in recruiting activated T cells into sites of tissue inflammation. To determine the in vivo function of IP-10, we constructed an IP-10-deficient mouse (IP-10\u2212\/\u2212) by targeted gene disruption. Immunological analysis revealed that IP-10\u2212\/\u2212 mice had impaired T cell responses. T cell proliferation to allogeneic and antigenic stimulation and IFN-\u03b3 secretion in response to antigenic challenge were impaired in IP-10\u2212\/\u2212 mice. In addition, IP-10\u2212\/\u2212 mice exhibited an impaired contact hypersensitivity response, characterized by decreased ear swelling and reduced inflammatory cell infiltrates. T cells recovered from draining lymph nodes also had a decreased proliferative response to Ag restimulation. Furthermore, IP-10\u2212\/\u2212 mice infected with a neurotropic mouse hepatitis virus had an impaired ability to control viral replication in the brain. This was associated with decreased recruitment of CD4+ and CD8+ lymphocytes into the brain, reduced levels of IFN-\u03b3 and the IFN-\u03b3-induced chemokines monokine induced by IFN-\u03b3 (Mig, CXCL9) and IFN-inducible T cell \u03b1 chemoattractant (I-TAC, CXCL11) in the brain, decreased numbers of virus-specific IFN-\u03b3-secreting CD8+ cells in the spleen, and reduced levels of demyelination in the CNS. Taken together, our data suggest a role for IP-10 in both effector T cell generation and trafficking in vivo.<\/jats:p>","DOI":"10.4049\/jimmunol.168.7.3195","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T20:08:54Z","timestamp":1398024534000},"page":"3195-3204","source":"Crossref","is-referenced-by-count":964,"title":["IFN-\u03b3-Inducible Protein 10 (IP-10; CXCL10)-Deficient Mice Reveal a Role for IP-10 in Effector T Cell Generation and Trafficking"],"prefix":"10.1093","volume":"168","author":[{"given":"Jennifer H","family":"Dufour","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"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle","family":"Dziejman","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":"Michael T","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Biochemistry, University of California , Irvine, CA 92697"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Josephine H","family":"Leung","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":"Thomas E","family":"Lane","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Biochemistry, University of California , Irvine, CA 92697"}],"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":[[2002,4,1]]},"reference":[{"key":"2026020209070980700_R1","first-page":"672","volume-title":"Nature","year":"1985"},{"key":"2026020209070980700_R2","first-page":"1373","volume-title":"J. 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