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- W4313381625 abstract "Abstract Crohn’s Disease is characterized by dysregulation of the immune response in the ileum. To study the perturbation of homeostasis within the ileum we utilize a “Bigenic” mouse model combining a TCR transgene and matching transgenic target antigen restricted to ileal crypt expression. Juvenile Bigenic mice experience TH17-associated ileitis and ileal hyperplasia. Antigen transcript is demonstrated to be localized exclusively in ileal crypts, as visualized with in situ hybridization of mRNA. Roughly 50% of Bigenic mice mature and acquire symptomatic phenotype (BigenicS) including colitis and suboptimal growth, while losing ileal hyperplasia. The remaining non-symptomatic Bigenic mice (BigenicNS) retain ileal hyperplasia and successfully build a supply of TH17 and ileal-reactive Treg cells. Previous studies in our lab indicate that IL-17A and INFγ are protective in this Bigenic model – their depletion by antibody binding accelerates disease and hinders accumulation of ileal-reactive Tregs. Furthermore, INFγKO Bigenic mice demonstrate almost complete penetrance of the symptomatic phenotype, with near 100% fatality by 50 days of life. Manipulation of microbiota in juvenile INFγKO Bigenic mice can protect them from this dysregulated state. Administration of a streptomycin/bacitracin antibiotic cocktail ad libitum in drinking water upon initial manifestation of weight loss symptoms or initiated preemptively upon weaning rescues and prevents, respectively, the weight loss phenotype and colitis." @default.
- W4313381625 created "2023-01-06" @default.
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- W4313381625 date "2018-05-01" @default.
- W4313381625 modified "2023-09-27" @default.
- W4313381625 title "In TH17-associated ileal inflammation, IFNγ and IL-17A support mucosal homeostasis and modulate self-tolerance" @default.
- W4313381625 doi "https://doi.org/10.4049/jimmunol.200.supp.172.9" @default.
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