{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T18:41:46Z","timestamp":1793299306586,"version":"4.5.0"},"reference-count":49,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2003,5,1]],"date-time":"2003-05-01T00:00:00Z","timestamp":1051747200000},"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":[[2003,5,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>T cell-mediated liver diseases are associated with elevated serum levels of C-C chemokine ligand 2 (CCL2)\/monocyte chemoattractant protein-1 (MCP-1). However, the extent to which the actions of CCL2\/MCP-1 contribute to the pathogenesis of T cell-mediated hepatitis remains incompletely understood. Con A-induced hepatitis is a liver-specific inflammation mediated by activated T cells and is driven by an up-regulation of the hepatic expression of TNF-\u03b1, IFN-\u03b3, and IL-4. The present study examined the role of CCL2\/MCP-1 in the pathogenesis of T cell-mediated hepatitis induced by Con A administration in the mouse. We demonstrate a novel hepatoprotective role for CCL2\/MCP-1 during Con A-induced hepatitis, because CCL2\/MCP-1 neutralization strikingly enhanced hepatic injury, both biochemically and histologically, after Con A administration. Furthermore, CCL2\/MCP-1 neutralization was associated with a significant reduction in the hepatic levels of TNF-\u03b1 and IFN-\u03b3, but with a significant increase in hepatic IL-4 levels. Moreover, IL-4 production and CCR2 expression by Con A-stimulated CD3+NK1.1+ T cells was significantly reduced by rMCP-1 treatment in vitro. In summary, we propose that CCL2\/MCP-1 fulfills a novel anti-inflammatory role in T cell-mediated hepatitis by inhibiting CD3+NK1.1+ T cell-derived IL-4 production through direct stimulation of its specific receptor CCR2. These findings may have direct clinical relevance to T cell-mediated hepatitis.<\/jats:p>","DOI":"10.4049\/jimmunol.170.10.5252","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T19:31:23Z","timestamp":1398022283000},"page":"5252-5259","source":"Crossref","is-referenced-by-count":48,"title":["C-C Chemokine Ligand 2\/Monocyte Chemoattractant Protein-1 Directly Inhibits NKT Cell IL-4 Production and Is Hepatoprotective in T Cell-Mediated Hepatitis in the Mouse"],"prefix":"10.1093","volume":"170","author":[{"given":"Maureen N","family":"Ajuebor","sequence":"first","affiliation":[{"name":"Liver Unit, Gastrointestinal Research Group, Faculty of Medicine, University of Calgary , Calgary, Alberta ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cory M","family":"Hogaboam","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Michigan Medical School , Ann Arbor, MI 48109"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tai","family":"Le","sequence":"additional","affiliation":[{"name":"Liver Unit, Gastrointestinal Research Group, Faculty of Medicine, University of Calgary , Calgary, Alberta ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark G","family":"Swain","sequence":"additional","affiliation":[{"name":"Liver Unit, Gastrointestinal Research Group, Faculty of Medicine, University of Calgary , Calgary, Alberta ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2003,5,15]]},"reference":[{"key":"2026020210102316600_R1","first-page":"806","volume-title":"Hum. 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