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- W2900181278 abstract "Abstract Dipeptidyl peptidase-4 (DPP4) is well known as a post-prandial blood glucose regulating protein by inactivation of incretin hormones. DPP4 also regulates T cell activation by interacting with adenosine deaminase. We investigated the role of hematopoietic DPP4 in T cell-mediated vascular inflammation and atherosclerosis. DPP4 highly expressed on the plasma membrane of T cells especially CD4+ T cells. DPP4 expression increased on circulating T cells in atherosclerotic patients (% DPP4+ CD4+ T cells: 27.46 ± 2.67 vs. 48.06 ± 1.96 for healthy control vs. atherosclerotic patients, p<0.0001). Deficiency of DPP4 on hematopoietic cells protected Ldlr−/− mice from high fat diet-induced atherosclerosis progression and reduced T cell infiltration in aortic plaque. Aorta from Ldlr−/− mice with Dpp4−/− bone marrows showed a much less DPP4 expression, suggesting bone marrow derived cells are the major sources of DPP4 within the aorta. Transwell® migration assay showed T cells with high migratory activity had higher levels of DPP4 expression. Both in vitro and in vivo migration assays suggest T cells deficient for DPP4 displayed a reduced migratory ability. Futher investigation suggests both enzymatic and non-enzymatic actions of DPP4 are involved in the regulation of T cell migration. Taken together, DPP4 increased on T cells in atherosclerosis and is important for T cell migratory activity, which promotes T cell-mediated vascular inflammation and atherosclerotic progression. Our results suggest an essential role for DPP4 in regulating T cell migration." @default.
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- W2900181278 date "2016-05-01" @default.
- W2900181278 modified "2023-10-06" @default.
- W2900181278 title "Dipeptidyl peptidase-4 promotes T cell migration" @default.
- W2900181278 doi "https://doi.org/10.4049/jimmunol.196.supp.54.1" @default.
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