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- W4313381963 abstract "Abstract Inflammatory bowel disease (IBD) is a common, chronic, progressive inflammatory intestinal disease in the world. The etiology of IBD is due to the imbalance of host immune responses to intestinal flora. Many human genes play the important role to induce improper immune responses, including IL-10, STAT3, IRGM, AGT16L1, NOD2 and RUNX3. It has been reported that homozygous Runx3-ko mice develop colitis spontaneously. However, homozygous Runx3-ko mice show very high mortality rate in the first 2 week of life, and are hard to study the role of Runx3 in the spontaneous colitis. A mouse pedigree (spontaneous colitis, SC) carried an ENU-induced Tyr301stop point mutation of Runx3, which resulted in a short form truncated form of Runx3. SC mice started to show spontaneous diarrhea after weaning. SC mice exhibited prominant enlargement of colon that revealed large amounts of inflammatory cells infiltration from mucosal to muscular layers. Immunofluorescent staining showed large amounts of CD4+ T cells involved in the inflammatory colon. Moreover, inflammatory colons of SC mice expressed higher mRNA levels of IL-17A, and serum IL-17A level were also upregulated in SC mice. In addition, SC CD4+ T cells expressed stronger IL-17A than WT CD4+ T cells after in vitro activation. Transfer of total SC CD4+ T cells into Rag1-ko host mice resulted in autoimmune colitis. In summary, C-terminal truncated Runx3 results in autoimmune colitis through elevated Th17 immune responses. Thus, the SC mouse model is a valuable tool for investigations on the effect of immune system upon spontaneous colitis." @default.
- W4313381963 created "2023-01-06" @default.
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- W4313381963 date "2017-05-01" @default.
- W4313381963 modified "2023-09-27" @default.
- W4313381963 title "ENU-induced C-terminal truncation of Runx3 results in Th17-associated autoimmune colitis" @default.
- W4313381963 doi "https://doi.org/10.4049/jimmunol.198.supp.217.11" @default.
- W4313381963 hasPublicationYear "2017" @default.
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