{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:15:38Z","timestamp":1791296138401,"version":"4.1.0"},"reference-count":48,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":2069,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2010,1]]},"abstract":"<jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      <jats:bold>Stress-induced soluble major histocompatibility complex class I\u2013related chains A\/B (MIC A\/B) are increased in chronic liver diseases and hepatocellular malignancy. We investigated the impact of these molecules on liver injury, apoptosis, and fibrosis in nonalcoholic steatohepatitis (NASH). Blood and liver tissue were obtained from 40 patients with NASH undergoing bariatric surgery for obesity. The control group consisted of 10 healthy individuals. We also investigated 10 patients with nonalcoholic fatty liver (NAFL). Polymerase chain reaction was used to measure messenger RNA (mRNA) transcripts of MIC A\/B, natural killer cell receptor G2D (NKG2D), CD95\/Fas, and tumor necrosis factor\u2013related apoptosis-inducing ligand (TRAIL)\u2013death receptor 5 (DR5). Apoptosis was quantified by way of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) (intrahepatic) and M30\/M65 (systemic). Liver injury was assessed histopathologically and serologically (alanine aminotransferase\/aspartate aminotransferase). Fibrosis was identified by Sirius red staining, quantitative morphometry, and \u03b1-smooth muscle actin and collagen 1\u03b1 transcripts. Compared with controls, patients with NASH revealed significant increases in (1) NKG2D mRNA (13.1-fold) and MIC A\/B mRNA (3.6-fold and 15.8-fold, respectively); (2) TRAIL\u2013DR5 and CD95\/Fas mRNA (2.7-fold and 3.6-fold, respectively); (3) TUNEL-positive hepatocytes (4.0-fold); and (4) M30 and M65 levels (4.6-fold and 3.4-fold, respectively). We found relevant correlations between MIC protein expression rates and NAS and fibrosis stages. In contrast, NKG2D and MIC A\/B transcripts were attenuated in patients with NAFL compared with NASH. Histopathologically, NASH patients revealed increased NAS scores, an accumulation of natural killer cells, and 2.7-fold increased hepatic fibrosis by quantitative morphometry.<\/jats:bold>\n                      <jats:bold>Conclusion:<\/jats:bold>\n                      <jats:bold>Our findings suggest an important role for MIC A\/B in liver injury. Therapeutic intervention aimed at reducing MIC A\/B levels may beneficially affect the progression of NASH. (Hepatology 2009.)<\/jats:bold>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/hep.23253","type":"journal-article","created":{"date-parts":[[2009,12,8]],"date-time":"2009-12-08T14:02:26Z","timestamp":1260280946000},"page":"92-102","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":104,"title":["Major Histocompatibility Complex Class I\u2013Related Chains A and B (Mic A\/B): A Novel Role in Nonalcoholic 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