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- W4313355026 startingPage "65.6" @default.
- W4313355026 abstract "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 reduced in the ileums of premature infants with NEC, it is unknown whether they play a critical function in preventing NEC. This study investigated Treg development in newborn rat pups and their function in regulating 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. The results revealed that there were few Treg numbers in the terminal ileums of newborn rats and 8-fold reduction after NEC (p=0.002). Adoptive transfer of Tregs significantly improved weight loss, survival from 53% to 88%, and NEC incidence from 87% to 35% (p<0.05). The Tregs suppressed the upregulation of costimulatory molecule CD80 on dendritic cells and inhibited the trafficking of effector cells from leaving the MLN. These findings suggest that 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 a therapeutic potential in the prevention of NEC." @default.
- W4313355026 created "2023-01-06" @default.
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- W4313355026 date "2013-05-01" @default.
- W4313355026 modified "2023-09-27" @default.
- W4313355026 title "Protective function of FoxP3+ regulatory T cells in experimental necrotizing enterocolitis (P1010)" @default.
- W4313355026 doi "https://doi.org/10.4049/jimmunol.190.supp.65.6" @default.
- W4313355026 hasPublicationYear "2013" @default.
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