Inflammatory bowel disease (IBD) arises from complex interactions between genes, the immune system, the microbiome, and environmental triggers. Further research must be done because a significant proportion of IBD patients do not respond to current treatments. There is an increasing array of mouse IBD models with their own advantages and disadvantages. One model alone will not fully replicate human IBD; therefore, researchers must consider the pros and cons of each model in relation to the mechanism of action they are investigating.
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