{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T22:01:27Z","timestamp":1790546487658,"version":"4.1.0"},"reference-count":18,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2005,7,1]],"date-time":"2005-07-01T00:00:00Z","timestamp":1120176000000},"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":[[2005,7,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The liver has an enormous capacity to regenerate in response to insults, but the cellular events and molecules involved in liver regeneration are not well defined. In this study, we report that ligands expressed on the surface of lymphocytes have a substantial effect on liver homeostasis. We demonstrate that a T cell-restricted ligand, homologous to lymphotoxin, exhibits inducible expression, competes with herpesvirus glycoprotein D for herpesvirus entry mediator on T cells (LIGHT), signaling through the lymphotoxin receptor (LT\u03b2R) expressed on mature hepatocytes induces massive hepatomegaly. Using genetic targeting and a receptor fusion protein, we further show that mice deficient in LT\u03b2R signaling have a severe defect in their ability to survive partial hepatectomy with marked liver damage and failure to initiate DNA synthesis after partial hepatectomy. We further show that mice deficient in a LT\u03b2R ligand, LT\u03b1, also show decreased ability to survive partial hepatectomy with similar levels of liver damage and decreased DNA synthesis. Therefore, our study has revealed an unexpected role of lymphocyte-restricted ligands and defined a new pathway in supporting liver regeneration.<\/jats:p>","DOI":"10.4049\/jimmunol.175.2.1295","type":"journal-article","created":{"date-parts":[[2014,4,22]],"date-time":"2014-04-22T22:40:18Z","timestamp":1398206418000},"page":"1295-1300","source":"Crossref","is-referenced-by-count":68,"title":["Contribution of the Lymphotoxin \u03b2 Receptor to Liver Regeneration"],"prefix":"10.1093","volume":"175","author":[{"given":"Robert A","family":"Anders","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Chicago , Chicago, IL 60637"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sumit K","family":"Subudhi","sequence":"additional","affiliation":[{"name":"Committee on Immunology, University of Chicago , Chicago, IL 60637"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Wang","sequence":"additional","affiliation":[{"name":"Committee on Immunology, University of Chicago , Chicago, IL 60637"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Klaus","family":"Pfeffer","sequence":"additional","affiliation":[{"name":"Institut fur Medizinische Mikrobiologie, Heinrich-Heine-Universit , Dusseldorf ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang-Xin","family":"Fu","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Chicago , Chicago, IL 60637"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2005,7,15]]},"reference":[{"key":"2026020212150256600_R1","first-page":"60","volume-title":"Science","year":"1997"},{"key":"2026020212150256600_R2","first-page":"e301","volume-title":"Front Biosci.","year":"2002"},{"key":"2026020212150256600_R3","first-page":"117","volume-title":"Mech. 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