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| Content Provider | Springer Nature Link |
|---|---|
| Author | Xu, Q. Cao, J. S. Zhang, X. M. |
| Copyright Year | 2002 |
| Abstract | Objective and design: To explore the mechanisms by which liver-infiltrating T lymphocytes cause hepatocyte damage in the liver injury induced by delayed-type hypersensitivity to picryl chloride.¶Materials and methods: Nonparenchymal cells (NPC) were isolated 12 h after liver injury elicitation and fractionated into Kupffer cell-enriched (Fr. A) and lymphocyte-enriched populations (Fr. B). They were used as the effectors for co-culture with hepatocytes.¶Results: The cells in total NPC and Fr. B harvested at 12 h of liver injury were increased two- and six-fold respectively compared with those at 0 h. Fr. B, mainly including CD4+ and CD8+ T cells, exhibited a significantly stronger hepatotoxicity than total NPC did, while Fr.A did not. NPC at 12 h showed remarkably increased matrix metalloproteinase-2 and -9 activities indicative of infiltration potential through extracellular matrix. When NPC and hepatocytes were cultured in separated compartments in Transwell chamber, no hepatotoxicity was observed. However, 30 min-pre-contact with hepatocytes as stimulator significantly triggered NPC hepatotoxicity. The acquisition of such hepatotoxic potential was significantly abolished by anti-LFA-1 pretreatment for NPC or anti-ICAM-1 treatment for hepatocytes before contact. Both aprotonin and superoxide dismutase dose-dependently inhibited the hepatotoxicity.¶Conclusions: Liver-infiltrating T lymphocytes may be triggered by hepatocytes via LFA-1/ICAM-1 interaction to release toxic substances, such as proteases and oxygen radicals, which consequently lead to the hepatocyte damage. |
| Starting Page | 44 |
| Ending Page | 50 |
| Page Count | 7 |
| File Format | |
| ISSN | 10233830 |
| Journal | Inflammation Research |
| Volume Number | 51 |
| Issue Number | 1 |
| e-ISSN | 1420908X |
| Language | English |
| Publisher | Birkhäuser Verlag |
| Publisher Date | 2002-01-01 |
| Publisher Place | Basel |
| Access Restriction | One Nation One Subscription (ONOS) |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology Immunology |
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