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- W2061628804 abstract "Necrotizing enterocolitis (NEC) results from severe intestinal inflammation in premature infants. FoxP3+ regulatory T cells (Tregs) are central to gut homeostasis. While Tregs are significantly reduced in the ileum of premature infants with NEC, it is unknown whether they play a critical function in preventing NEC. This study investigates whether Treg development is delayed in newborn rat pups and whether Tregs play a protective role in experimental NEC induction. Utilizing a rat model of experimental NEC, the ontogeny of T cells and Tregs in newborn pups was characterized by flow cytometry. To investigate the functions of Tregs, newborn pups were given Tregs harvested from adult rats prior to NEC induction to assess clinical improvement and mechanisms of immune regulation. There were few Tregs in the mesenteric lymph nodes (MLN) and ileums of newborn rats, which were further reduced after NEC. Adoptive transfer of Tregs significantly improved weight loss, survival from 53% to over 85%, and intestinal damage based on preservation of cellular composition and reduction of NEC score from maximum of 3 to 1 in severity. The Tregs suppressed the upregulation of costimulatory molecule CD80 on dendritic cells (DCs) and regulated the trafficking of effector cells in the MLN. There is a developmental delay in Tregs which contributes to the excessive inflammatory state in NEC. Adoptive transfer of Tregs attenuates the induction of NEC by regulating DCs and modulating effector cell trafficking. Treg immunotherapy has an enormous therapeutic potential in the prevention and treatment of NEC." @default.
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- W2061628804 date "2013-02-01" @default.
- W2061628804 modified "2023-09-26" @default.
- W2061628804 title "Protective Function of FoxP3+ Regulatory T Cells in Experimental Necrotizing Enterocolitis" @default.
- W2061628804 doi "https://doi.org/10.1016/j.jaci.2012.12.701" @default.
- W2061628804 hasPublicationYear "2013" @default.
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