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Masako Murai, Hiroyuki Yoneyama, Akihisa Harada, Zhang Yi, Christian Vestergaard, Baoyu Guo, Kenji Suzuki, Hitoshi Asakura, Kouji Matsushima
J Clin Invest. 1999;
104(1):49
doi:10.1172/JCI6642
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e examined the molecular pathogenesis of graft-versus-host disease–associated (GVHD-associated) liver injury in mice, focusing on the role of chemokines. At the second week after cell transfer in the parent-into-F1 model of GVHD, CD8+ T cells — especially donor-derived CD8+ T cells — infiltrated the liver, causing both portal hepatitis and nonsuppurative destructive cholangitis (NSDC). These migrating cells expressed CCR5. Moreover, macrophage inflammatory protein-1α (MIP-1α), one of the ligands for CCR5, was selectively expressed on intralobular bile duct epithelial cells, endothelial cells, and infiltrating macrophages and lymphocytes. Administration of anti-CCR5 antibody dramatically reduced the infiltration of CCR5+CD8+ T lymphocytes into the liver, and consequently protected against liver damage in GVHD. The levels of Fas ligand (FasL) mRNA expression in the liver were also decreased by anti-CCR5 antibody treatment. Anti–MIP-1α antibody treatment also reduced liver injury. These results suggest that MIP-1α–induced migration of CCR5-expressing CD8+ T cells into the portal areas of the liver plays a significant role in causing liver injury in GVHD; thus, CCR5 and its ligand may be the novel target molecules of therapeutic intervention of hepatic GVHD.
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