| Literature DB >> 20080065 |
Chisato Saeki1, Masanori Nakano, Hiroki Takahashi, Saburo Saito, Sadamu Homma, Hisao Tajiri, Mikio Zeniya.
Abstract
Participation of Tregs in the generation of autoimmune hepatic inflammation (AHI) was examined using a newly established dendritic cell (DC)-based mouse model of hepatitis. The inflammatory activity of AHI peaked 21 days after DC vaccination. Forkhead box P3 (Foxp3) expression on day 21 was significantly increased in the liver but was decreased in the spleen. CD4(+)CD25(+) Tregs from the liver on day 21 showed inhibitory activity against the proliferation of CD4(+)CD25(-) T cells. On day 21, the expression of CXCR3 on Tregs and its ligand CXCL9 in hepatic tissue was upregulated, and levels of mRNA of transforming growth factor (TGF)-beta and IL-2, essential for Treg differentiation, in the liver were also increased. Suppression of AHI activity by prednisolone treatment decreased Treg accumulation in the liver. Accumulation of Tregs might occur through Treg recruitment mediated by CXCR3/CXCL9 interaction and expansion in the liver by upregulated TGF-beta and IL-2. Copyright 2009 Elsevier Inc. All rights reserved.Entities:
Mesh：
Substances：
Year: 2010 PMID： 20080065 DOI： 10.1016/j.clim.2009.12.002
Source DB: PubMed Journal: Clin Immunol ISSN： 1521-6616 Impact factor: 3.969