Abstract：
BACKGROUND:Accumulating evidence suggests that Foxp3+ regulatory T (Treg) cells act as inhibitory mediators of inflammation; however, the in vivo mechanism underlying this protection remains elusive in liver diseases. AIMS:To clarify the in vivo role of Foxp3+ Treg cells in liver fibrosis, we used the DEREG mouse, which expresses the diphtheria toxin receptor under control of the Foxp3 promoter, allowing for specific deletion of Foxp3+ Treg cells. METHODS:Bile duct ligation-induced liver injury and fibrosis were assessed by histopathology, fibrogenic gene expression, and measurement of cytokine and chemokine levels. RESULTS:Depletion of Foxp3+ Treg cells enhanced Th17 cell response as demonstrated by the increase of IL-17+ cells and related gene expressions including Il17f, Il17ra, and Rorgt in the fibrotic livers of DEREG mice. Of note, infiltration of CD8+ T cells and Cd8 gene expression was significantly increased in the livers of DEREG mice. Consistent with increased IL-17+ and CD8+ T cell responses, DEREG mice generated higher levels of inflammatory cytokines (TNF-α, IL-6, and IL-12p70) and chemokines (MCP-1, MIP-1α, and RANTES). These results were concordant with severity of liver fibrosis and hepatic enzyme levels (ALT and ALP). CONCLUSIONS:The present findings demonstrate that Foxp3+ Treg cells inhibit the profibrogenic inflammatory milieu through suppression of pro-fibrogenic CD8+ and IL-17+ T cells.
journal_name
Dig Dis Scijournal_title
Digestive diseases and sciencesauthors
Roh YS,Park S,Lim CW,Kim Bdoi
10.1007/s10620-014-3438-2subject
Has Abstractpub_date
2015-07-01 00:00:00pages
2009-18issue
7eissn
0163-2116issn
1573-2568journal_volume
60pub_type
杂志文章abstract：:The clonality of gastric glands remains a controversial topic. Chimeric mouse studies suggested that all gastric glands were monoclonal. However, using the X-linked transgenic mouse model, we have suggested that most glands are polyclonal during development and that the fraction of monoclonal glands increases after bi...
journal_title：Digestive diseases and sciences
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