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CD4(+)CD25(+) T cells have been identified as a population of immunoregulatory T cells, which mediate suppression of CD4(+)CD25(-) T cells by cell-cell contact and not secretion of suppressor cytokines. In this study, we demonstrated that CD4(+)CD25(+) T cells do produce high levels of transforming growth factor (TGF)-beta1 and interleukin (IL)-10 compared(More)
Molecular mechanisms regulating TGF-β induction of Foxp3 expression and thus induction of iTregs has been the focus of a great deal of study in recent years. It has become clear that this process is influenced by a number of factors as perhaps might be predicted by the fact that there is an overarching need of the immune system to fine-tune response to(More)
Infection of the stomach with Helicobacter pylori is an important risk factor for gastritis, peptic ulcer, and gastric carcinoma. Although it has been well established that persistent colonization by H. pylori is associated with adaptive Th1 responses, the innate immune responses leading to these Th1 responses are poorly defined. Recent studies have shown(More)
Interleukin (IL)-10 and transforming growth factor (TGF)-␤ 1 are suppressor cytokines that frequently occur together during a regulatory T cell response. Here we used a one gene doxy-cycline (Dox)-inducible plasmid encoding TGF-␤ 1 to analyze this association and test its utility. In initial studies, we showed that intranasal administration of this plasmid(More)
Nucleotide oligomerization domain (NOD)2 is a member of the NOD-like receptor family of proteins that initiate inflammatory responses when exposed to ligands derived from bacterial components that gain access to the intracellular milieu. It is thus somewhat paradoxical that polymorphisms in the gene that encode NOD2 (CARD15) that lead to impaired NOD2(More)
In this study, we show that a single intranasal dose of a plasmid encoding active transforming growth factor ␤ 1 (pCMV-TGF-␤ 1) prevents the development of T helper cell type 1 (Th1)-mediated experimental colitis induced by the haptenating reagent, 2,4,6-trinitrobenzene sul-fonic acid (TNBS). In addition, such plasmid administration abrogates TNBS colitis(More)
It is well established that polymorphisms of the caspase activation and recruitment domain 15 (CARD15) gene, a major risk factor in Crohn's disease (CD), lead to loss of nucleotide-binding oligomerization domain 2 (NOD2) function. However, a molecular explanation of how such loss of function leads to increased susceptibility to CD has remained unclear. In a(More)
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