Abstract
Inflammatory bowel disease is a disease that reflects a disequilibrium in host–commensal homeostasis. T-bet−/−×RAG2−/− deficient mice develop a spontaneous juvenile ulcerative colitis resulting from a pro-inflammatory response to the commensal microbiota that is dendritic cell and TNF-α driven [schematized in Fig. 1]. The TRUC (T-bet−/− RAG2−/− ulcerative colitis) model is discussed in the broader context of the adaptive and innate immune mechanisms that regulate host–commensal relationships within the intestine.
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